Journal articles on the topic 'Index of α-expression'
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Chen, Yung-Che, Po-Yuan Hsu, Mao-Chang Su, Chien-Hung Chin, Chia-Wei Liou, Ting-Ya Wang, Yong-Yong Lin, Chiu Ping Lee, Meng-Chih Lin, and Chang-Chun Hsiao. "miR-21-5p Under-Expression in Patients with Obstructive Sleep Apnea Modulates Intermittent Hypoxia with Re-Oxygenation-Induced-Cell Apoptosis and Cytotoxicity by Targeting Pro-Inflammatory TNF-α-TLR4 Signaling." International Journal of Molecular Sciences 21, no. 3 (February 3, 2020): 999. http://dx.doi.org/10.3390/ijms21030999.
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The purpose of this study is to explore the anti-inflammatory role of microRNAs (miR)-21 and miR-23 targeting the TLR/TNF-α pathway in response to chronic intermittent hypoxia with re-oxygenation (IHR) injury in patients with obstructive sleep apnea (OSA). Gene expression levels of the miR-21/23a, and their predicted target genes were assessed in peripheral blood mononuclear cells from 40 treatment-naive severe OSA patients, and 20 matched subjects with primary snoring (PS). Human monocytic THP-1 cell lines were induced to undergo apoptosis under IHR exposures, and transfected with miR-21-5p mimic. Both miR-21-5p and miR-23-3p gene expressions were decreased in OSA patients as compared with that in PS subjects, while TNF-α gene expression was increased. Both miR-21-5p and miR-23-3p gene expressions were negatively correlated with apnea hypopnea index and oxygen desaturation index, while TNF-α gene expression positively correlated with apnea hypopnea index. In vitro IHR treatment resulted in decreased miR-21-5p and miR-23-3p expressions. Apoptosis, cytotoxicity, and gene expressions of their predicted target genes—including TNF-α, ELF2, NFAT5, HIF-2α, IL6, IL6R, EDNRB, and TLR4—were all increased in response to IHR, while all were reversed with miR-21-5p mimic transfection under IHR condition. The findings provide biological insight into mechanisms by which IHR-suppressed miRs protect cell apoptosis via inhibit inflammation, and indicate that over-expression of the miR-21-5p may be a new therapy for OSA.
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Li, Xi-Ying, Yan-Ting Yang, Yue Zhao, Xie-He Kong, Guang Yang, Jue Hong, Dan Zhang, and Xiao-Peng Ma. "Moxibustion Inhibits the Expression of Colonic NLRP3 through miR7/RNF183/NF-κB Signaling Pathway in UC Rats." Evidence-Based Complementary and Alternative Medicine 2021 (November 3, 2021): 1–12. http://dx.doi.org/10.1155/2021/6519063.
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Background. Moxibustion has been recognized as an effective approach for ulcerative colitis, yet its mechanism is not clear. The research aimed to investigate the influence of moxibustion on the activation of NLRP3 inflammasome and its mechanism in treating ulcerative colitis by observing miR7/RNF183 inducing IκB α ubiquitination to regulate NF-κB signaling pathway in an ulcerative colitis rat model. Methods. An ulcerative colitis rat model was established by unlimited access to self-administration of 3.5% (w/v) dextran sulfate sodium solution. Mild moxibustion was applied to bilateral Tianshu points (ST25) in the moxa-stick moxibustion group; rats in the control group were intervened by intraperitoneal injection of ubiquitination inhibitor, MG132. The disease activity index was determined at the end of the intervention; colon injury was observed and scored after hematoxylin-eosin staining; the immunohistochemical method was adopted to detect the expressions of colonic IL-1β and NLRP3 proteins; Western blot determined the expressions of RNF183, IκB α, and NF-κB p65 proteins in the colon; the immunofluorescence test was used to observe the coexpression of IκB α/ubiquitin and IκB α/RNF183 proteins in the colon; immunoprecipitation assay was adopted to observe the interaction between IκB α and RNF183 proteins; and quantitative real-time polymerase chain reaction determined the expression of colonic miR7. Results. Moxibustion lowered the disease activity index, manifesting as restored colonic tissue and reduced inflammatory reaction, and decreased expression levels of NLRP3 and IL-1β proteins, compared with the model group. It also reduced colonic expression of NF-κB p65 protein, together with the increased level of IκB α protein and weaker expression levels of ubiquitin and RNF183 proteins and mRNAs and stronger expression of miR7. There were no significant differences between the moxa-stick moxibustion group and the control group except the expressions of RNF183 protein and mRNA and miR7. Conclusion. Moxibustion encourages the recovery of colon injury probably by regulating the expression of NLRP3 protein in ulcerative colitis rats through miR7/RNF183/NF-κB signaling pathway.
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Alexiou, George A., George Vartholomatos, Kalliopi Stefanaki, Amalia Patereli, Lefkothea Dova, Achilleas Karamoutsios, George Lallas, George Sfakianos, Maria Moschovi, and Neofytos Prodromou. "Expression of heat shock proteins in medulloblastoma." Journal of Neurosurgery: Pediatrics 12, no. 5 (November 2013): 452–57. http://dx.doi.org/10.3171/2013.7.peds1376.
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Object Medulloblastoma (MB) is the most common malignant brain tumor in children. Heat shock proteins (HSPs) comprise a superfamily of proteins that serve as molecular chaperones and are overexpressed in a wide range of human cancers. The purpose of the present study was to investigate the expression of HSP27 (pSer82), HSP27 (pSer15), HSP40, HSP60, HSP70, HSP90-α, Akt, and phospho-Akt by multiplex bead array assay of MBs. The results of HSP and Akt expression were correlated with MB subtype; immunohistochemical expression of Ki-67 index, bcl-2, and p53; and patients' prognosis. Methods The authors retrospectively evaluated 25 children with MB who underwent surgery. Immunohistochemical analysis of Ki-67, p53, and bcl-2 expression was performed in all cases. By using multiplex bead array assay, a simultaneous detection of HSP27 (pSer82), HSP27 (pSer15), HSP40, HSP60, HSP70, HSP90-α, Akt, and phospho-Akt was performed. Results Medulloblastoma with extensive nodularity had significantly lower HSP27 (pSer15) expression (p = 0.039) but significantly higher HSP60 expression (p = 0.021) than classic MB. Large-cell MB had significantly higher HSP70 expression (p = 0.028) than classic MB. No significant difference was found between HSP27 (pSer82), HSP40, HSP90-α, Akt, or phospho-Akt expression and MB subtype. Large-cell MBs had significantly higher Ki-67 index compared with classic MBs (p = 0.033). When analyzing all MBs, there was a significant negative correlation between HSP27 (pSer15) and Ki-67 index (r = −0.475, p = 0.016); a significant positive correlation between HSP70 expression and Ki-67 index (r = 0.407, p = 0.043); and a significant positive correlation between HSP70 expression and bcl-2 index (r = 0.491, p = 0.023). Patients with large-cell MB had a worse survival than those with classic MB, but the difference did not reach statistical significance (p = 0.076). Conclusions A substantial expression of several HSPs in MB was observed. Given that HSPs represent an attractive strategy for anticancer therapy, further studies, involving larger series of patients, are obviously necessary to clarify the relationship of HSPs with tumor aggressiveness and prognosis.
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Jankowski, J., R. McMenemin, D. Hopwood, J. Penston, and K. G. Wormsley. "Abnormal expression of growth regulatory factors in Barrett's oesophagus." Clinical Science 81, no. 5 (November 1, 1991): 663–68. http://dx.doi.org/10.1042/cs0810663.
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1. In order to assess potential abnormalities in the control of mucosal proliferation, 30 patients with Barrett's oesophagus were studied in order to evaluate the presence and distribution of epidermal growth factor, transforming growth factor-α and epidermal growth factor receptor to determine the Ki-67 labelling index in the affected oesophageal mucosa. Serial sections were analysed immunohistochemically. Ten of the patients had adenocarcinoma in the Barrett's mucosa and the other 20 had differing histological types of Barrett's mucosa (10, intestinal-type; 10, fundic-or cardiac-type). 2. The expression of transforming growth factor-α, epidermal growth factor and epidermal growth factor receptor was increased and the Ki-67 labelling index was higher in Barrett's mucosa compared with normal gastric mucosa. The ‘intestinal-type’ of Barrett's mucosa had the greatest expression of transforming growth factor-α, epidermal growth factor receptor and the highest Ki-67 labelling index compared with the other types of Barrett's metaplasia. Five cases of ‘intestinal-type’ Barrett's metaplasia had especially high Ki-67 labelling indices and these patients over-expressed both transforming growth factor-α and epidermal growth factor receptor. The patients with adenocarcinomas in the Barrett's mucosa also over-expressed transforming growth factor-α and epidermal growth factor receptor, but not epidermal growth factor, compared with normal gastric mucosa. 3. In conclusion, both normal gastric mucosa and Barrett's mucosa have potential autocrine growth regulatory mechanisms, but Barrett's mucosa has increased expression of both of the measured ligands and of the epidermal growth factor receptor.
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Qian, Xiao-Xian, Chen-Wen Cai, Han-Yang Li, Li-Jie Lai, Dong-Juan Song, Yu-Qi Qiao, Jun Shen, and Zhi-Hua Ran. "Transcribed ultraconserved region (T-UCR) uc.261 expression is closely correlated with disease activity and intestinal permeability in Crohn’s disease." Therapeutic Advances in Gastroenterology 12 (January 2019): 175628481988073. http://dx.doi.org/10.1177/1756284819880733.
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Objectives: Transcribed ultraconserved region (T-UCR) uc.261 is reported to participate in intestinal mucosa barrier damage in Crohn’s disease (CD). The aim of this study was to determine the association with disease activity and intestinal permeability. Methods: Uc.261 level in colon mucosa and Harvey-Bradshaw Index (HBI) were evaluated in 20 active CD patients. Uc.261 expression and transepithelial electrical resistance (TEER) were determined in Caco2 and T84 cells treated with tumor necrosis factor alpha (TNF-α), respectively. Body weight, disease activity index (DAI), colon length, histological index (HI), intestinal permeability to FITC-dextran, uc.261, and tight junction proteins (TJPs) levels were evaluated in BALB/C mice treated with saline enema, trinitrobenzene sulfonic acid (TNBS)/ethanol enema, and anti-TNF-α monoclonal antibody injection, respectively. Results: Uc.261 expression was overexpressed in CD patients, TNF-α treated cells, and colitis mice. Uc.261 expression was positively correlated with HBI ( r = 0.582, p = 0.007) in CD patients, and positively correlated with TNF-α concentration and negatively correlated TEER in Caco2 and T84 cells (all p < 0.05). Furthermore, uc.261 was positively correlated with DAI ( r = 0.824, p = 0.008), HI ( r = 0.672, p = 0.021), and intestinal permeability ( r = 0.636, p = 0.012), while negatively correlated with body weight ( r = –0.574, p = 0.035), colon length ( r = –0.866, p = 0.017), and TJP expression (all p < 0.05) in colitis mice. Conclusions: Uc.261 expression was closely correlated with disease activity and intestinal permeability in CD. Anti-TNF-α treatment may play its role through suppressing uc.261 expression in colitis mice.
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Nieto, A., L. Peña, M. D. Pérez-Alenza, M. A. Sánchez, J. M. Flores, and M. Castaño. "Immunohistologic Detection of Estrogen Receptor Alpha in Canine Mammary Tumors: Clinical and Pathologic Associations and Prognostic Significance." Veterinary Pathology 37, no. 3 (May 2000): 239–47. http://dx.doi.org/10.1354/vp.37-3-239.
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Eighty-nine canine mammary tumors and dysplasias of 66 bitches were investigated to determine the immunohistochemical expression of classical estrogen receptor (ER-α) and its clinical and pathologic associations and prognostic value. A complete clinical examination was performed and reproductive history was evaluated. After surgery, all animals were followed-up for 18 months, with clinical examinations every 3–4 months. ER-α expression was higher in tumors of genitally intact and young bitches ( P < 0.01, P < 0.01) and in animals with regular estrous periods ( P = 0.03). Malignant tumors of the bitches with a previous clinical history of pseudopregnancy expressed significantly more ER-α ( P = 0.04). Immunoexpression of ER-α decreased significantly with tumor size ( P = 0.05) and skin ulceration ( P = 0.01). Low levels of ER-α were significantly associated with lymph node involvement ( P < 0.01). Malignant tumors had lower ER-α expression than did benign tumors ( P < 0.01). Proliferation index measured by proliferating cell nuclear antigen immunostaining was inversely correlated with ER-α scores ( P = 0.05) in all tumors. Low ER-α levels in primary malignant tumors were significantly associated with the occurrence of metastases in the follow-up ( P = 0.03). Multivariate analyses were performed to determine the prognostic significance of some follow-up variables. ER-α value, Ki-67 index, and age were independent factors that could predict disease-free survival. Lymph node status, age, and ER-α index were independent prognostic factors for the overall survival. The immunohistochemical detection of ER-α in canine mammary tumors is a simple technique with prognostic value that could be useful in selecting appropriate hormonal therapy.
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Dong, Weitao, Bin Wang, Rongchao Zhang, Junyi Cao, and Rong Wu. "Therapeutic effects of acupuncture in rheumatoid arthritis are associated with centromere protein F expression." Allergologia et Immunopathologia 50, no. 3 (May 1, 2022): 47–54. http://dx.doi.org/10.15586/aei.v50i3.564.
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Rheumatoid arthritis is a globally common autoimmune inflammatory disease found especially in China. Acupuncture (AP), a traditional Chinese medicine (TCM) treatment method, is commonly used for treating rheumatoid arthritis. Many studies have demonstrated that acupuncture alone or in combination with other treatments is beneficial to treat clinical situation of rheumatoid arthritis, thus improving function and quality of life. In this study, we found that centromere protein F (CENPF) is a key gene in rheumatoid arthritis with acupuncture treatment by using differentially expressed genes (DEGs) and random forest model analysis of GSE57983 and GSE77298. Acupuncture helps to up-regulate the expression of CENPF in tissues in rheumatoid arthritis. Functionally, overexpression of CENPF inhibits monocyte chemoattractant protein (MCP)-1, tumor necrosis factor (TNF)-α, and Interleukin (IL)-6 expressions whereas deficiency of CENPF facilitates MCP-1, TNF-α, and IL-6 expressions in a collagen-induced arthritis (CIA) rat model. Furthermore, knocked down CENPF with acupuncture treatment antagonizes the inhibition of MCP-1, TNF-α, and IL-6 expressions in a CIA rat model. CENPF could be a crucial biomarker in regulating function of acupuncture in treating rheumatoid arthritis. Objective: The objective of this study is to study the critical role of CENPF in regulation of rheumatoid arthritis with acupuncture treatment. Methods: PCA was used to analyze the different expression genes between AP treatment group and control group. Volcano plot and random forest model were used to analyze the decreased and increased expression genes. RT-qPCR and IF were used to measure the expression of CENPF in CIA model rat with or without AP treatment. The expression of MCP-1, TNF-α and IL-6 was measured by western blotting. The pathology character and arthritis index were used to analyze the severity of joint injury. Results: PCA data showed that the expression of genes was different between AP treatment group and control group from GEO datasets. Volcano plot and random forest model analysis indicated that CENPF is the most significantly increased expression gene after AP treatment. RT-qPCR and IF assay showed that CENPF is reduced expression in CIA model rat, while CENPF is upregulated expression in CIA model rat with AP treatment. Furthermore, overexpression of CENPF reduced the increasing of MCP-1, TNF-α and IL-6 in CIA model rat. On the contrary, CENPF deficiency induced the expression of MCP-1, TNF-α and IL-6 in CIA model rat. Additionally, the expression of MCP-1, TNF-α and IL-6 in CIA model rat was suppressed, whereas knockdown of CENPF antagonized the decrease of MCP-1, TNF-α and IL-6 in CIA model rat with AP treatment. Conclusions: CENPF may be a key gene in regulation of the therapeutic effects of acupuncture in rheumatoid arthritis.
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Wang, Shih-Wei, Tsun-Mei Lin, Chiou-Huey Wang, Hsiao-Han Liu, and Jer-Yiing Houng. "Increased Toll-Like Receptor 2 Expression in Peptidoglycan-Treated Blood Monocytes Is Associated with Insulin Resistance in Patients with Nondiabetic Rheumatoid Arthritis." Mediators of Inflammation 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/690525.
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The close relationship between increased TLR-2 expression in blood monocytes and insulin resistance in RA patients is shown in this study. Traditional risk factors for metabolic disorders, including the waist circumstance, body mass index (BMI), triglyceride (TG), and ratio of TG to high density lipoprotein (HDL) cholesterol, were closely correlated with HOMA (homoeostasis model assessment) index in patients with nondiabetic RA. Expressions of TLR2 in peripheral blood monocytes, following stimulation with peptidoglycan which is known as a TLR2 agonist, were closely correlated with the HOMA index, TNF-α, and IL-6 concentrations. Accordingly, TLR-2 receptor and its related inflammatory cytokines could be potential therapeutic targets in managing insulin resistance in RA patients.
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Wang, Rubiao, Wenjun Xie, Hongrong Rao, Yujian Tan, Rongkun Liao, Yingmei Jiang, and Hongbin Zhang. "Effects of Tanshinone on Hemodynamics and Expression of NF- B and Myeloperoxidase in Rats with Spinal Cord Ischemia-Reperfusion Injury." Journal of Biomaterials and Tissue Engineering 10, no. 7 (July 1, 2020): 1040–45. http://dx.doi.org/10.1166/jbt.2020.2347.
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Spinal cord ischemia-reperfusion injury (SCII) can cause spinal nerve injury and loss of function. Tanshinone IIA has antioxidant activity. However, the effect of tanshinone on SCII rats remains unclear. SD rats were randomly divided sham operation group (sham group), SCII group and tanshinone group. Heart rhythm (HR), mean blood pressure (MAP), and myocardial oxygen consumption index (RPP) hemodynamic parameters were analyzed. Rat neurological function scores were performed by the Tarlov method. The glutamate detection kit was used to detect the content of glutamate, superoxide dismutase (SOD) and myeloperoxidase (MPO). NF-κ B protein expression was assessed by Western blot. The expressions of tumor necrosis factor-α (TNF-α) and interleukin6 (IL-6) were analyzed by ELISA. In SCII group, HR, MAP, RPP, and neurological function score as well as SOD activity were significantly decreased with increased MPO, glutamate, TNF-α and IL-6 secretion as well as elevated NF-κ B expression compared with sham group (P < 0 05). After tanshinone treatment, HR, MAP, RPP, and neurological function score as well as SOD activity were all significantly increased along with decreased MPO, glutamate, TNF-α and IL-6 secretion, as well as reduced NF- κB expression compared with SCII group (P < 0 05). Tanshinone can improve the oxidative stress, reduce the secretion of inflammatory factors, and improve hemodynamics which is possibly through regulating NF-κ B expression.
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Oregón-Romero, Edith, Mónica Vázquez-Del Mercado, Sandra Luz Ruiz-Quezada, Rosa Elena Navarro-Hernández, Héctor Rangel-Villalobos, Gloria Martínez-Bonilla, Ana Guilaisne Bernard-Medina, Juan Armendáriz-Borunda, Jesús García-Bañuelos, and José Francisco Muñoz-Valle. "Tumor Necrosis Factor α-308 and -238 Polymorphisms in Rheumatoid Arthritis. Association With Messenger RNA Expression and sTNF-α." Journal of Investigative Medicine 56, no. 7 (October 1, 2008): 937–43. http://dx.doi.org/10.2310/jim.0b013e318189152b.
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BackgroundRheumatoid arthritis (RA) is characterized by a progressive joint damage mediated mainly by tumor necrosis factor α (TNFα). We investigated the relationship of TNFα-308 and -238 polymorphisms with messenger RNA (mRNA) expression and soluble TNFα (sTNFα) in 50 RA and 100 healthy subjects (HS).MethodsClinical and laboratory assessments were performed. Spanish Health Assessment Questionnaire Disability Index, Spanish version of Arthritis Impact Measurement Scales and Disease Activity Score using 28 joint count indices were applied to RA patients. The TNFα-308 and -238 polymorphisms were performed by polymerase chain reaction and restriction fragment length polymorphism techniques. The mRNA expression of TNFα was quantified by real-time polymerase chain reaction. The sTNFα levels were measured by enzyme-linked immunosorbent assay.ResultsThe TNFα-308 polymorphism showed an increased frequency of guanine (G)/adenine (A) genotype in RA versus HS (P = 0.03; 95% confidence interval, 1.05-8.08; odds ratio, 2.9) and also the A allele was more frequent in RA patients versus HS (P = 0.04; 95% confidence interval, 1.01-7.29; odds ratio, 2.7). The G/G genotype and also the G allele were more frequent in HS. No significant difference was observed in TNFα-238 polymorphism. Rheumatoid arthritis patients showed high TNFα mRNA expression (1.33-fold). The G/G genotype was associated with high mRNA and sTNFα levels in both TNFα polymorphisms. The correlation of sTNFα levels with C-reactive protein, erythrocyte sedimentation rate, rheumatoid factor, Spanish Health Assessment Questionnaire Disability Index, and Spanish version of Arthritis Impact Measurement Scales, was observed.ConclusionThe TNFα-308 polymorphism is a susceptibility marker to RA. The G/G genotype is associated with a high mRNA and soluble TNFα expression.
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Venkataraman, Balaji, Saeeda Almarzooqi, Vishnu Raj, Pradeep K. Dudeja, Bhoomendra A. Bhongade, Rajesh B. Patil, Shreesh K. Ojha, Samir Attoub, Thomas E. Adrian, and Sandeep B. Subramanya. "α-Bisabolol Mitigates Colon Inflammation by Stimulating Colon PPAR-γ Transcription Factor: In Vivo and In Vitro Study." PPAR Research 2022 (April 13, 2022): 1–22. http://dx.doi.org/10.1155/2022/5498115.
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The incidence and prevalence of inflammatory bowel disease (IBD, Crohn’s disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α-bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α-bisabolol interacts with PPAR-γ, which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α-bisabolol interacts with PPAR-γ, a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α-bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α-Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β, TNF-α, and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α-bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκB) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β/δ expression was not altered, indicating α-bisabolol is a specific stimulator of PPAR-γ. α-Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β/δ in pretreated in LPS-stimulated RAW264.7 macrophages. α-Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α-bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression.
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Xu, Zhiyu, Xiaohong Xie, Jia Tian, Huajie Wang, Zhenlin Lei, and Zhongyan Zhao. "Down-Regulation of Mir-21 Alleviates Lung Injury Induced by Burns Through Activating Silent Mating Type Information Regulation 2 Homolog 1 (SIRT1)-Protein Kinase B (AKT)-Nuclear Factor κB (NF- κB) Pathway." Journal of Biomaterials and Tissue Engineering 10, no. 4 (April 1, 2020): 576–81. http://dx.doi.org/10.1166/jbt.2020.2295.
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Severe burns can cause lung damage. Mir-21 is a promising biomarker for inflammatory response. However, the expression and role of Mir-21 in lung injury have not been elucidated. SD rats were divided into control group; model group; Mir-21 inhibition group; Mir-21 inhibition + SIRT1 inhibitor (nicotinamide) group followed by analysis of Mir-21 expression by real time PCR, arterial blood gas index and lung wet-to-dry weight ratio, lung tissue MPO and SOD activities, protein content and cell count in bronchoalveolar lavage fluid, secretion of TNF-α and IL-2 by ELISA, SIRT1 expression by Real time PCR and ELISA and Akt and NF-κB level by Western blot. Compared with control group, model group showed significantly decreased PaO2 and pH, increased W/D and MPO activity increased, decreased SOD activity, increased protein content and cell count in BALF, Mir-21 expression, and secretion of TNF-α and IL-2, decreased SIRT1 expression, and promoted pAkt and NF-κB expression (P < 0 05). Down-regulation of Mir-21 significantly improved blood gas index, decreased W/D and MPO activity, increased SOD activity, decreased TNF-α and IL-2 secretion; increased SIRT1 expression, and decreased pAkt and NF-κB expression (P < 0 05). However, SIRT1 inhibitor significantly reversed the effect of down-regulation of Mir-21 on the protection of lung injury. Downregulation of Mir-21 regulates SIRT1-Akt-NFκB pathway and oxidative stress, reduces inflammation, and thus alleviates burn-induced lung injury, and may be a new option for treating acute lung injury.
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Soares, Vanessa Nogueira, Aline Klug Radke, Maria Ângela André Tillmann, Andréa Bittencourt Moura, and Luis Osmar Braga Schuch. "Physiological performance of rice seeds treated with thiamethoxam or rhizobacteria under different temperatures." Journal of Seed Science 36, no. 2 (June 2014): 186–93. http://dx.doi.org/10.1590/2317-1545v32n2925.
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This study aimed to evaluate, at 15, 20 and 25 ºC, the physiological potential and enzyme activity of seedlings from six samples of rice seeds stored for one year and treated with growth-promoting rhizobacteria (Pseudomonas synxantha) and the bioactivator thiametoxam. The following were evaluated: seed germination, first germination count, root protrusion speed index, emergence percentage and emergence speed index, shoot and root length and enzyme activity (esterases, α-amylase and peroxidases) at 15, 20 and 25 ºC. In these conditions, thiametoxam and the rhizobacteria P. synxantha (DFs 185) improved the physiological performance of rice seeds with physiological qualities at low temperatures (20 and 15 ºC) and did not change the expression of the esterase and peroxidase isoenzymes. The rhizobacteria P. synxantha (DFs 185) increased the expression of the enzyme α-amylase at low temperatures.
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Shaker, Olfat G., Shereen O. Tawfic, Amira M. El-Tawdy, Mohamed H. M. El-Komy, Manal El Menyawi, and Ahmed A. Heikal. "Expression of TNF-α, April and BCMA in Behcet’s Disease." Journal of Immunology Research 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/380405.
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Background. Tumor necrosis factor-alpha (TNF-α) is an important proinflammatory cytokine which plays an important role in the immunopathogenesis of Behcet’s disease (BD). B cell activating factor (BAFF) and its homolog A proliferation inducing ligand (APRIL) are members of the tumor necrosis factor family. BAFF binds to 3 receptors, B cell activating factor receptor (BAFF-R), transmembrane activator and calcium modulator ligand interactor (TACI), and B cell maturation antigen (BCMA) that are expressed by B cells.Objective. Estimation of the serum levels of TNF-α, APRIL, BAFF, and BCMA in patients with BD in an effort to evaluate their degree of involvement in the pathogenesis and development of BD.Patients and Methods. This study included 30 male patients fulfilling the international study group criteria for the diagnosis of BD. Twenty age-matched healthy male volunteers served as control. Serum samples were used for quantification of TNF-α, APRIL, BCMA, BAFF, and hsCRP using ELISA techniques.Results. The mean serum levels of TNF-α, APRIL, BCMA, and BAFF were more elevated in cases than in controls in a statistically significant manner(P<0.001). Positive correlation was observed between hs-CRP and BDCAF (Behcet’s disease current activity forum) index (r0.68,P<0.001). None of the TNF family members tested was affected by a positive pathergy test.Conclusions. Patients have significantly higher levels of TNF family members’ (TNF-α, BAFF, APRIL, and BCMA) compared to controls which might contribute to the pathogenesis of BD.
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Báez, Francisco, Belén Gómez, Victoria de Brun, Nélida Rodríguez-Osorio, and Carolina Viñoles. "Effect of Ethanol on Parthenogenetic Activation and α-Tocopherol Supplementation during In Vitro Maturation on Developmental Competence of Summer-Collected Bovine Oocytes." Current Issues in Molecular Biology 43, no. 3 (December 16, 2021): 2253–65. http://dx.doi.org/10.3390/cimb43030158.
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The use of α-tocopherol during in vitro maturation (IVM) is an alternative to minimize the adverse effects of heat stress on oocyte competence. However, α-tocopherol is diluted in ethanol, which can induce oocyte parthenogenetic activation (PA). This study aimed to evaluate the role of ethanol concentration on PA and the effect of α-tocopherol supplementation during IVM on the developmental competence and the expression of key genes in blastocysts derived from summer-collected oocytes. All in vitro embryo production was conducted at 5% O2, 5% CO2 at 38.5 °C. Experiment 1: oocytes were cultured with or without 0.05% ethanol. As positive PA control matured oocytes were subjected to 3% or 7% ethanol for 7 min. Oocytes from all groups were placed in fertilization medium (22 h) and culture medium (9 days). Ethanol at 0.05% during IVM did not induce oocyte PA, however, 3% and 7% ethanol were effective parthenogenetic inductors. Experiment 2: oocytes were cultured in maturation medium supplemented with 0, 50, 100 and 200 μM α-tocopherol, diluted in 0.05% ethanol. After in vitro fertilization and embryo culture, we assessed blastocyst apoptotic index and the transcription of a panel of genes. The results showed that supplementation with 100 μM α-tocopherol reduced apoptotic index and increased the expression of SOD2. In conclusion, 100 μM α-tocopherol, diluted in 0.05% ethanol, can be used during IVM to embryonic quality.
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Jin, Hongkui, Renhui Yang, Wei Li, Hsienwie Lu, Anne M. Ryan, Annie K. Ogasawara, John Van Peborgh, and Nicholas F. Paoni. "Effects of exercise training on cardiac function, gene expression, and apoptosis in rats." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (December 1, 2000): H2994—H3002. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2994.
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This study determined the effects of exercise training on cardiac function, gene expression, and apoptosis. Rats exposed to a regimen of treadmill exercise for 13 wk had a significant increase in cardiac index and stroke volume index and a concomitant decrease in systemic vascular resistance compared with both age-matched and body weight-matched sedentary controls in the conscious state at rest. In exercise-trained animals, there was no change in the expression of several marker genes known to be associated with pathological cardiac adaptation, including atrial natriuretic factor, β-myosin heavy chain, α-skeletal and smooth muscle actins, and collagens I and III. Exercise training, however, produced a significant induction of α-myosin heavy chain, which was not observed in rats with myocardial infarction. No histological features of cardiac apoptosis were observed in the treadmill-trained rats. In contrast, apoptotic myocytes were detected in animals with myocardial infarction. In summary, exercise training improves cardiac function without evidence of cardiac apoptosis and produces a pattern of cardiac gene expression distinct from pathological cardiac adaptation.
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Xu, Guangmeng, Yajuan Sun, Huaiqiang He, Qiuli Xue, Yajie Liu, and Lihua Dong. "Effect of TrkB-PLC/IP3 pathway on intestinal inflammatory factors and enterocyte apoptosis in mice with colitis." Acta Biochimica et Biophysica Sinica 52, no. 6 (May 22, 2020): 675–82. http://dx.doi.org/10.1093/abbs/gmaa044.
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Abstract In this study, we aimed to explore the effect of TrkB-PLC/IP3 pathway on intestinal inflammatory factors and enterocyte apoptosis in mice with colitis. The mouse model of ulcerative colitis was established by medication, and 40 SPF C57BL/6J mice (8 weeks old) were randomly divided into normal group (healthy mice, n = 10), control group (sham-operated mice, n = 10), model group (model mice without any treatment, n = 10), and K252a group (model mice treated with 100 μmol/kg TrkB-PLC/IP3 pathway inhibitor for 5 days before clysis, n = 10). The results showed that mice in the model and K252a groups, as compared with normal and control groups, had no significant changes in the levels and protein expressions of serum tumor necrosis factor-α (TNF-α) and TNF-γ in the colon tissues (P>0.05), and had a significant increase in disease activity index, colon mucosa damage index, tissue damage index scores, and levels and protein expressions of serum interleukin-4 (IL-4) and IL-8, but had a significant decrease in the level and protein expression of serum IL-10 (P<0.05). Mice in the model and K252a groups showed blocked enterocyte cycle progression, elevated apoptosis ratio, and significantly increased mRNA and protein expressions of Caspase3, Bax, FasL, and Fas, but significantly reduced mRNA and protein expressions of p-TrkB, PLC-γ1, IP3, and Bcl-2 (P<0.05). Moreover, intestinal inflammation and apoptosis induced by colitis in the K252a group became more aggravated by inhibiting the activity of TrkB-PLC/IP3 pathway. In conclusion, inhibition of TrkB-PLC/IP3 pathway can increase the expression of intestinal inflammatory factors and promote enterocyte apoptosis in mice with colitis.
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Colegrove, K. M., F. M. D. Gullanda, D. K. Naydan, and L. J. Lowenstine. "Tumor Morphology and Immunohistochemical Expression of Estrogen Receptor, Progesterone Receptor, p53, and Ki67 in Urogenital Carcinomas of California Sea Lions (Zalophus californianus)." Veterinary Pathology 46, no. 4 (March 9, 2009): 642–55. http://dx.doi.org/10.1354/vp.08-vp-0214-c-fl.
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Metastatic carcinoma of urogenital origin is a common cause of mortality in free-ranging California sea lions (Zalophus californianus). The etiology of this cancer is likely multifactorial, with viral infection, genetic factors, and exposure to environmental organochlorine contaminants possible contributing factors. In this study, expression of estrogen receptor α (ER α), progesterone receptor (PR), p53, and Ki67 were evaluated by immunohistochemistry in 12 sea lions with metastatic carcinoma, genital epithelial dysplasia, and intraepithelial neoplasia; 4 with genital epithelial dysplasia and intraepithelial neoplasia without metastases; and 6 control animals. Dysplastic and neoplastic lesions were identified in multiple areas of the cervix, vagina, penis, prepuce, and urethra in affected animals, suggesting multicentric development. Lesions were graded according to degree of epithelial dysplasia and infiltration and lesions of different grades were evaluated separately. Estrogen receptor expression was lower in intraepithelial lesions compared with normal genital epithelium, and expression in metastatic lesions was completely absent. There was progesterone receptor expression in neoplastic cells in intraepithelial lesions of all grades and in metastases, with no significant difference between lesion grades or between control and affected epithelium. Ki67 index and p53 expression increased with lesion grade and were higher in lesions than normal epithelium. Metastatic tumors exhibited highly variable morphology; however, proliferation index, ER α, PR, and p53 expression were similar in tumors with different patterns of growth. These results suggest that endogenous hormones, environmental contaminants that interact with steroid hormone receptors, and alterations in p53 may play a role in urogenital carcinogenesis in California sea lions.
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Koyanagi, Satoru, Hinako Suyama, Yukako Kuramoto, Noaya Matsunaga, Hiroshi Takane, Shinji Soeda, Hiroshi Shimeno, Shun Higuchi, and Shigehiro Ohdo. "Glucocorticoid Regulation of 24-Hour Oscillation in Interferon Receptor Gene Expression in Mouse Liver." Endocrinology 147, no. 11 (November 1, 2006): 5034–40. http://dx.doi.org/10.1210/en.2006-0415.
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Although the antiviral effect of interferon (IFN) varies depending on 24-h oscillation in the expression of its specific receptor, the mechanism of oscillation remains to be clarified. Here we report that oscillation in the expression of the IFN receptor gene (IFN-α/β R1) in mouse liver is caused by the endogenous rhythm of glucocorticoid secretion. Brief exposure of mouse hepatic cells (Hepa 1–6) to corticosterone (CORT) resulted in a significant decrease in mRNA levels of IFN-α/β R1. The CORT-induced decrease in IFN-α/β R1 mRNA levels was reversed by pretreating the cells with RU486, a glucocorticoid receptor antagonist. The mRNA levels of IFN-α/β R1 gene in the liver of adrenalectomized mice were consistently increased throughout the day. However, a single administration of CORT to adrenalectomized mice significantly decreased the mRNA levels of IFN-α/β R1 in the liver. Furthermore, the rhythmic phase of IFN-α/β R1 expression was modulated after the alteration of rhythmicity in glucocorticoid secretion, which was induced by restricted daily feeding. As a consequence, under manipulation of the feeding schedule, 2′-5′ oligoadenylate synthase activities, as an index of antiviral effect, in plasma and liver at 24 h after IFN-α injection also varied depending on the alteration of glucocorticoid secretion rhythm. These results suggest that the endogenous rhythm of glucocorticoid secretion is involved in the circadian regulation of IFN-α/β R1 expression in mouse liver. Our findings also support the notion that monitoring the 24-h variation in IFN receptor function is useful for selecting the most appropriate time of day to administer IFN.
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Watanabe, Takako, Naoya Sakamoto, Mina Nakagawa, Sei Kakinuma, Yasuhiro Itsui, Yuki Nishimura-Sakurai, Mayumi Ueyama, et al. "Inhibitory Effect of a Triterpenoid Compound, with or without Alpha Interferon, on Hepatitis C Virus Infection." Antimicrobial Agents and Chemotherapy 55, no. 6 (March 28, 2011): 2537–45. http://dx.doi.org/10.1128/aac.01780-10.
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ABSTRACTA lack of patient response to alpha interferon (α-IFN) plus ribavirin (RBV) treatment is a major problem in eliminating hepatitis C virus (HCV). We screened chemical libraries for compounds that enhanced cellular responses to α-IFN and identified a triterpenoid, toosendanin (TSN). Here, we studied the effects and mechanisms of action of TSN on HCV replication and its effect on α-IFN signaling. We treated HCV genotype 1b replicon-expressing cells and HCV-J6/JFH-infected cells with TSN, with or without α-IFN, and the level of HCV replication was quantified. To study the effects of TSN on α-IFN signaling, we detected components of the interferon-stimulated gene factor 3 (ISGF3), phosphorylated signal transducer and activator of transcription 1 (STAT1), and STAT2 by Western blotting analysis; expression levels of mRNA of interferon regulatory factor 9 using real-time reverse transcription-PCR (RT-PCR); and interferon-stimulated response element reporter activity and measured the expression levels of interferon-inducible genes for 2′,5′-oligoadenylate synthetase, MxA, protein kinase R, and p56 using real-time RT-PCR. TSN alone specifically inhibited expression of the HCV replicon (50% effective concentration = 20.6 nM, 50% cytotoxic concentration > 3 μM, selectivity index > 146). Pretreatment with TSN prior to α-IFN treatment was more effective in suppressing HCV replication than treatment with either drug alone. Although TSN alone did not activate the α-IFN pathway, it significantly enhanced the α-IFN-induced increase of phosphorylated STATs, interferon-stimulated response element activation, and interferon-stimulated gene expression. TSN significantly increased baseline expression of interferon regulatory factor 9, a component of interferon-stimulated gene factor 3. Antiviral effects of treatment with α-IFN can be enhanced by pretreatment with TSN. Its mechanisms of action could potentially be important to identify novel molecular targets to treat HCV infection.
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Pu, Jiaojiao, Rui Wang, Guanglin Zhang, and Ju Wang. "FGF-7 facilitates the process of psoriasis by inducing TNF-α expression in HaCaT cells." Acta Biochimica et Biophysica Sinica 51, no. 10 (September 6, 2019): 1056–63. http://dx.doi.org/10.1093/abbs/gmz095.
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Abstract The purpose of this study was to uncover the mechanism of tumor necrosis factor (TNF)-α induction by fibroblast growth factor-7 (FGF-7) in human HaCaT cells and the potential role of FGF-7-specific antibody F-9 in psoriatic therapy. TNF-α expression in HaCaT cells induced by FGF-7 was analyzed by quantitative polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assays. In vivo, the BALB/c mouse psoriasis model established by topical application of imiquimod (IMQ) was used to determine the role of FGF-7-specific antibody (F-9) in skin inflammation. We found that induction of TNF-α expression by FGF-7 in HaCaT cells was suppressed by FGF-7-specific antibody F-9. Western blot analysis results showed that FGF-7 induced TNF-α expression in HaCaT cells via the FGF receptor 2 (FGFR2)/AKT/NF-κB signaling pathway. In vivo, F-9 could significantly ameliorate the inflammations in a mouse psoriatic model evaluated by Psoriasis Area and Severity Index scores and ear thickness, which was consistent with the results of hematoxylin–eosin staining, immunohistochemistry assay, and western blot analysis. These results indicate that FGF-7 induces TNF-α expression in HaCaT cells and FGF-7 antibody F-9 alleviates IMQ-induced psoriasiform in mice. Therefore, FGF-7/FGFR2 signaling pathway is a potential target for psoriasis treatment.
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Dwianingsih, Ery Kus, Yudha Mathan Sakti, Rahadyan Magetsari, David Yosua Parulian Hutahaean, Galih Prasetya Sakadewa, Paramita Dyah Lasmana, Nicolaas C. Budhiparama, and Ery Kus Dwianingsih. "Correlation of Tumor Necrosis Factor-α Expression with Pain Level in Degenerative Lumbar Canal Stenosis Patients." Open Access Macedonian Journal of Medical Sciences 9, B (September 17, 2021): 1135–39. http://dx.doi.org/10.3889/oamjms.2021.6708.
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Introduction: Pain in degenerative lumbar canal stenosis is caused by osteoarthritis of a facet joint and intervertebral disc degeneration. Some inflammatory mediators such as tumor necrosis factor (TNF)-α are present in degenerative lumbar canal stenosis. This study aimed to evaluate the correlation of pain and functional pre-operative scores with the expression of TNF-α in nucleus pulposus, annulus fibrosus, and facet joint.
Methods: Patients diagnosed with degenerative lumbar canal stenosis and planned for surgical treatment were included in this study. Patients with history of fracture, neoplasm, and/or infection of the spine were excluded. Tissue samples were collected from the nucleus pulposus, annulus fibrosus, facet joint, flavum ligament and paraspinal muscles of the spine during the surgery. TNF-α expression was examined semi-quantitively and correlated with the axial and radicular pain that were measured using Visual Analog Score (VAS) score. The result was then statistically analyzed.
Results: The expression of TNF-α in the paraspinal muscle (6.30±14.20) was significantly higher compared to other locations. TNF-α expression in the facet joint group was significantly correlated with the intensity of low back pain measured by VAS score (r=0.893, p < 0.001), and pre-operative functional outcome based on Oswestry Disability Index (ODI) (r=0.948, p < 0.001).
Conclusion: TNF-α expression, especially in the facet joint, is significantly associated with the pain intensity and pre-operative ODI that allow pain reduction with less invasive treatment in lumbar canal stenosis patients.
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Bouchard, Luigi, Marie-Claude Vohl, Yves Deshaies, Caroline Rhéaume, Marleen Daris, and André Tchernof. "Visceral adipose tissue zinc finger protein 36 mRNA levels are correlated with insulin, insulin resistance index, and adiponectinemia in women." European Journal of Endocrinology 157, no. 4 (October 2007): 451–57. http://dx.doi.org/10.1530/eje-07-0073.
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Introduction: Adipose tissue is now recognized as an endocrine organ and secretes numerous molecules and proteins potentially involved in the physiopathology of the metabolic syndrome. Recently, we have determined the transcriptome of omental adipose tissue, leading to the identification of a new candidate gene for obesity-related metabolic complications, zinc finger protein 36 (ZFP36), which is known to down-regulate tumor necrosis factor-α TNF-α) expression. Objective: The objective of this study was to further examine the relationship between ZFP36 gene expression levels, obesity-related phenotypes, and adipokines. Methods: Abdominal subcutaneous and omental adipose tissue samples were obtained from 46 women undergoing elective gynecological surgery. Adipose tissue ZFP36 mRNA abundance was assessed by quantitative real-time PCR. Body fat accumulation and distribution were measured by dual X-ray absorptiometry and computed tomography. Fasting blood levels of glucose, insulin, and lipids, and circulating TNF-α, interleukin-6 (IL-6), resistin, and adiponectin were also measured. Results: No correlation was observed between s.c. ZFP36 mRNA levels and any of the phenotypes tested. However, although omental ZFP36 mRNA levels were not correlated with measures of body fatness and lipid profile, they were negatively correlated with fasting insulin levels (R = −0.31; P = 0.05), the insulin resistance index (HOMA-IR; R = −0.31; P = 0.05), and 2-h post-glucose insulinemia (R = −0.32; P = 0.05). Omental ZFP36 mRNA abundance was also positively correlated with adiponectinemia (R = 0.35; P = 0.03) but not with circulating TNF-α, IL-6, and resistin concentrations. Conclusion: These results suggest that ZFP36 gene expression in omental adipose tissue, but not in abdominal s.c. fat, may offer partial protection against the development of insulin resistance and diabetes.
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Ge, Ning, Qing Xia, Zhong-Hua Yang, Qun-Fang Ding, and Zhi Zeng. "Vascular Endothelial Injury and Apoptosis in Rats with Severe Acute Pancreatitis." Gastroenterology Research and Practice 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/235017.
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We explored mechanisms of vascular endothelial injury that lead to systemic multiple organ failure by detecting the soluble endothelial protein C receptor (sEPCR), von Willebrand factor (vWF), serum nitric oxide (NO), and tumor necrosis factor alpha (TNF-α) and Bcl-2 mRNA and Bax mRNA expression in a severe acute pancreatitis (SAP) rat model. Compared to controls, the levels of TNF-α, vWF, and sEPCR were significantly increased in the experimental group at 12 hours and 24 hours and the NO level was significantly decreased. After 12 hours, the aortic endothelial apoptosis index and Bax mRNA expression in aortic endothelial cells had increased in the experimental group, but Bcl-2 mRNA levels had decreased. All these changes appeared at both 12 h and 24 hours. The results indicated that vascular endothelial injury and apoptosis markers were elevated in SAP. Endothelial injury and increased apoptosis in the experimental group were related to the increased expression of TNF-α.
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Drake, W. M., D. M. Berney, K. Kovacs, and J. P. Monson. "Markers of cell proliferation in a GH-producing adenoma of a patient treated with pegvisomant." European Journal of Endocrinology 153, no. 2 (August 2005): 203–5. http://dx.doi.org/10.1530/eje.1.01961.
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We report our findings on markers of cell proliferation (Ki-67 labelling index and topoisomerase-α expression) in a somatotroph pituitary tumour before and after exposure to pegvisomant, a GH receptor antagonist developed for the treatment of acromegaly. Specimens from two separate pituitary operations, separated by a period of 17 years that included 4 years of pegvisomant treatment, were stained for markers of cellular proliferation. Ki-67 labelling index and topoisomerase-α expression were both markedly greater (1–3% compared with 0–0.5% and 15–80% compared with 2–10% respectively) in the pegvisomant-exposed tumour compared with the earlier specimen. Clearly, caution must be exercised when interpreting findings from a single case, particularly one sufficiently refractory to conventional therapies to require treatment with pegvisomant. However, our data reinforce the requirement for careful radiological surveillance of the pituitary in the context of a drug that does not target the tumour responsible and where serum GH cannot serve as a marker of disease activity or tumour size.
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LI, JIE, HONGFU XIE, TING WEN, HONGBO LIU, WU ZHU, and XIANG CHEN. "Expression of High Mobility Group Box Chromosomal Protein 1 and Its Modulating Effects on Downstream Cytokines in Systemic Lupus Erythematosus." Journal of Rheumatology 37, no. 4 (January 28, 2010): 766–75. http://dx.doi.org/10.3899/jrheum.090663.
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Objective.To compare the expression of high mobility group box chromosomal protein 1 (HMGB1) and the modulating effects on its downstream cytokines in patients with systemic lupus erythematosus (SLE) and healthy controls.Methods.HMGB1 concentrations in serum from SLE patients and controls were measured by immunoblot analysis. HMGB1 messenger RNA (mRNA) expression in peripheral blood mononuclear cells (PBMC) was detected by real-time reverse transcription–polymerase chain reaction. Immunofluorescence assay was employed to examine the translocation of HMGB1 in monocytes after endotoxin stimulation. Release of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) by PBMC after rHMGB1 stimulation was also measured.Results.Serum HMGB1 levels and HMGB1 mRNA expressions in PBMC were elevated in SLE patients compared with controls. A positive correlation was demonstrated between HMGB1 concentrations and SLE Disease Activity Index. There was an inverse correlation between HMGB1 levels and C4 and C3 concentrations in SLE patients. HMGB1 concentrations were higher in patients with vasculitis and myositis. Lipopolysaccharide stimulated a temporarily elevated release of HMGB1 in SLE patients compared with controls. The pattern and localization of HMGB1 staining in monocytes were similar in both groups. After stimulation with rHMGB1, TNF-α level decreased but IL-6 level increased in SLE patients compared with controls.Conclusion.Our findings suggest that increased serum levels of HMGB1 in SLE may be associated with lupus disease activity. The altered production of TNF-α and IL-6 in response to rHMGB1 stimulation may participate in the disruption of cytokine homeostasis in SLE.
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Sohn, Young Bae, Min Jung Kwak, Su Jin Kim, Sung Won Park, Chi Hwa Kim, Mi Young Kim, Eun Kyung Kwon, Kyung Hoon Paik, and Dong-Kyu Jin. "Correlation of Adiponectin Receptor Expression with Cytokines and Insulin Sensitivity in Growth Hormone (GH)-Treated Children with Prader-Willi Syndrome and in Non-GH-Treated Obese Children." Journal of Clinical Endocrinology & Metabolism 95, no. 3 (March 1, 2010): 1371–77. http://dx.doi.org/10.1210/jc.2009-1489.
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Abstract Context: Prader-Willi syndrome (PWS), a genetic disorder characterized by obesity in early childhood, is reported to have elevated levels of adiponectin. The effects of adiponectin are mediated by adiponectin receptors (ADIPORs) that include ADIPOR1 and ADIPOR2. There is evidence that several cytokines, including adiponectin, TNF-α, and IL-6, are involved in insulin sensitivity. Objective and Methods: We measured the relative expression of adiponectin, ADIPORs, several proinflammatory cytokines including TNF-α, and IL-6 expression in peripheral blood mononuclear cells (PBMCs) of children with PWS and obese comparators using real-time PCR. Their correlation with homeostasis model assessment insulin resistance index (HOMA-IR) was analyzed. Patients: Thirty children with PWS (median age 7.1 yr, 18 males, 12 females) that were being treated with GH and 32 obese children not receiving GH treatment (median age 9.1 yr, 15 males, 17 females) for comparison were enrolled. Results: The PWS children had increased expression of ADIPOR2 (P = 0.02) and decreased expression of IL-6 (P = 0.03) compared with the comparison group. Moreover, there was a significant positive correlation between the ADIPORs and TNF-α (ADIPOR1 vs. TNF-α: r = 0.66, P < 0.001 in PWS, r = 0.80, P < 0.001 in comparison group; ADIPOR2 vs. TNF-α: r = 0.69, P < 0.001 in comparison group). The ADIPORs in the comparison group showed significant negative correlation with HOMA-IR (ADIPOR1 vs. HOMA-IR; ρ = −0.41, P = 0.02, ADIPOR2 vs. HOMA-IR; ρ = −0.46, P < 0.01). Conclusion: The results of this study showed that inflammatory cytokine expression was closely associated with the expression of the ADIPORs in the PBMCs of both the children with PWS and the comparison group. Moreover, ADIPOR2 expression was highly expressed in the PBMCs of the children with PWS. A further study on the mechanism of increased expression of ADIPOR2 and its correlation with the expression of TNF-α in the PBMCs using the non-GH-treated PWS and obese control will be warranted because this study compared GH-treated PWS with an obese comparator group.
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Kang, Xiuhong, Mengdi Jia, Luqing Zhao, and Shengsheng Zhang. "Bu-Zhong-Yi-Qi Granule Enhances Colonic Tight Junction Integrity via TLR4/NF-κB/MLCK Signaling Pathway in Ulcerative Colitis Rats." Evidence-Based Complementary and Alternative Medicine 2021 (March 9, 2021): 1–12. http://dx.doi.org/10.1155/2021/6657141.
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Background. Bu-zhong-yi-qi granule (BZYQ), a sort of Chinese herbal medicine, has exhibited therapeutic effects on ulcerative colitis (UC). However, the mechanism of BZYQ has not been fully clarified. This study was aimed at investigating the effects of BZYQ on UC rats model and at exploring its potential mechanism. Methods. The UC rats were established by enema of trinitrobenzene sulfonic acid (TNBS). The therapeutic effects of BZYQ treatment were evaluated by disease activity index (DAI), colon macroscopic damage index (CMDI) scores, and histological observation. The mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were measured by quantitative real time-polymerase chain reaction (qPCR). The expression of tight junction (TJ) proteins, occludin and claudin-1, in the colon was determined by Western blot and immunofluorescence. The expression of toll-like receptors 4 (TLR4), nuclear factor-kappa B (NF-κB), p-NF-κB, myosin light chain kinase (MLCK), MLC, and p-MLC levels in colon was determined by Western blot or qPCR. Results. The results showed that BZYQ could attenuate DAI, CMDI, and histological inflammation. TJ proteins expression was decreased in UC rats, but treatment with BZYQ restored the expression of occludin and claudin-1. In addition, BZYQ administration ameliorated UC-associated increase in the production of TNF-α, IL-1β, and the expression of TLR4, NF-κB, p-NF-κB, MLCK, MLC, and p-MLC, while BZYQ administration increased the production of IL-10. Conclusions. The therapeutic effect of BZYQ on UC is at least partially through regulation of the secretion of some inflammatory cytokines and improvement of TJ integrity via TLR4/NF-κB/MLCK pathway.
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S. Berguetti, Tandressa, Lucas S. P. Quintaes, Thais Hancio Pereira, Marcela Robaina, André Cruz, Raquel C. Maia, and Paloma de Souza. "TNF-α Modulates P-Glycoprotein Expression and Contributes to Cellular Proliferation via Extracellular Vesicles." Cells 8, no. 5 (May 24, 2019): 500. http://dx.doi.org/10.3390/cells8050500.
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P-glycoprotein (Pgp/ABCB1) overexpression is associated with multidrug resistance (MDR) phenotype and, consequently, failure in cancer chemotherapy. However, molecules involved in cell death deregulation may also support MDR. Tumor necrosis factor-alpha (TNF-α) is an important cytokine that may trigger either death or tumor growth. Here, we examined the role of cancer cells in self-maintenance and promotion of cellular malignancy through the transport of Pgp and TNF-α molecules by extracellular vesicles (membrane microparticles (MP)). By using a classical MDR model in vitro, we identified a positive correlation between endogenous TNF-α and Pgp, which possibly favored a non-cytotoxic effect of recombinant TNF-α (rTNF-α). We also found a positive feedback involving rTNF-α incubation and TNF-α regulation. On the other hand, rTNF-α induced a reduction in Pgp expression levels and contributed to a reduced Pgp efflux function. Our results also showed that parental and MDR cells spontaneously released MP containing endogenous TNF-α and Pgp. However, these MP were unable to transfer their content to non-cancer recipient cells. Nevertheless, MP released from parental and MDR cells elevated the proliferation index of non-tumor cells. Collectively, our results suggest that Pgp and endogenous TNF-α positively regulate cancer cell malignancy and contribute to changes in normal cell behavior through MP.
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Rasheed, H., MHM El-Komy, RA Hegazy, HI Gawdat, AM AlOrbani, and OG Shaker. "Expression of sirtuins 1, 6, tumor necrosis factor, and interferon-γ in psoriatic patients." International Journal of Immunopathology and Pharmacology 29, no. 4 (August 19, 2016): 764–68. http://dx.doi.org/10.1177/0394632016662475.
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Sirtuins (SIRT) have been regarded as culprits in the pathogenesis of various diseases. Their exact role has not been explained. This study aimed to assess the expression of SIRT1, SIRT6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ in psoriatic patients. Thirty psoriatic patients and 22 controls were enrolled. Clinical examination and Psoriasis Area and Severity Index (PASI) were obtained. Two skin biopsies (lesional, peri-lesional) and one from controls were obtained. Tissue levels of SIRT1, SIRT6, TNF-α, and IFN-γ were measured using ELISA. SIRT1 was significantly lower in lesional skin with gradual increase in perilesional followed by control skin ( P <0.001). SIRT6, TNF-α, and IFN-γ were significantly higher in lesional than perilesional and control skin ( P <0.001). Significant positive correlations were found between SIRT1 and TNF-α, IFN-γ and between SIRT6 and TNF-α in peri-lesional skin. SIRT1 and SIRT6 are potentially involved in the pathogenesis of psoriasis. Modulating their action could offer a novel therapy for such disease.
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Canales, Muna T., Meaghan Holzworth, Shahab Bozorgmehri, Areef Ishani, I. David Weiner, Richard B. Berry, Rebecca J. Beyth, and Michelle Gumz. "Clock gene expression is altered in veterans with sleep apnea." Physiological Genomics 51, no. 3 (March 1, 2019): 77–82. http://dx.doi.org/10.1152/physiolgenomics.00091.2018.
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Clock gene dysregulation has been shown to underlie various sleep disorders and may lead to negative cardio-metabolic outcomes. However, the association between sleep apnea (SA) and core clock gene expression is unclear. We performed a cross-sectional analysis of 49 Veterans enrolled in a study of SA outcomes in veterans with chronic kidney disease, not selected for SA or sleep complaints. All participants underwent full polysomnography and next morning whole blood collection for clock gene expression. We defined SA as an apnea-hypopnea index ≥15 events/h; nocturnal hypoxemia(NH) was defined as ≥10% of total sleep time spent at <90% oxygen saturation. We used quantitative real-time PCR to compare the relative gene expression of clock genes between those with and without SA or NH. Clock genes studied were Bmal1, Ck1δ, Ck1ε, Clock, Cry1, Cry2, NPAS2, Per1, Per2, Per3, Rev-Erb-α, RORα, and Timeless. Our cohort was 90% male, mean age was 71 yr (SD 11), mean body mass index was 30 kg/m2 (SD 5); 41% had SA, and 27% had NH. Compared with those without SA, Per3 expression was reduced by 35% in SA ( P = 0.027). Compared with those without NH, NPAS2, Per1, and Rev-Erb-α expression was reduced in NH (50.4%, P = 0.027; 28.7%, P = 0.014; 31%, P = 0.040, respectively). There was no statistical difference in expression of the remaining clock genes by SA or NH status. Our findings suggest that SA or related NH and clock gene expression may be interrelated. Future study of 24 h clock gene expression in SA is needed to establish the role of clock gene regulation on the pathway between SA and cardio-metabolic outcomes.
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Xu, Lili, Zhe Wang, and Lixiang Deng. "Effect of Vaspin on Myocardial Ischemia-Reperfusion Injury Rats and Expression of NLR Family Pyrin Domain Containing 3 (NLRP3)." Journal of Biomaterials and Tissue Engineering 10, no. 6 (June 1, 2020): 895–900. http://dx.doi.org/10.1166/jbt.2020.2342.
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Myocardial ischemia-reperfusion injury (MIRI) can cause myocardial damage. Vaspin can protect against myocardial damage. However, the effect of vaspin on MIRI rats and the expression of NLRP3 remains unclear. Sprague-Dawley rats were separated into sham group; MIRI group and Vaspin group, in which 100 ng/ml vaspin was administrated before model preparation followed by analysis of cardiac function by M-mode ultrasound, level of NLRP3, of type I collagen, IL-6 and TNF-α by ELISA, SOD activity and ROS by spectrophotometry and Bcl-2 and PI3K/AKT signaling protein expression by Western Blot. In MIRI group, left ventricular end-systolic diameter (LVESD), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), NLRP3 expression, contents of type I collagen, IL-6, TNF-α as well as ROS were significantly increased and SOD activity was significantly decreased with decreased Bcl-2 expression and upregulated pAKT and pPI3K (P < 0.05). In Vaspin group, LVESD, LVMI and LVEDD and NLRP3 expression as well as type I collagen, IL-6, TNF-α and ROS was decreased, SOD activity and Bcl-2 expression was significantly increased with downregulated pAKT and pPI3K (P < 0.05). Vaspin can regulate PI3K/AKT signaling pathway, inhibit NLRP3 expression, regulate oxidative stress, inhibit inflammation, reduce apoptosis, improve and improve cardiac function of myocardial ischemia-reperfusion injury in rats.
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McCarthy, Erin, Aaron Barron, Noelia Morales-Prieto, Martina Mazzocchi, Cathal M. McCarthy, Louise M. Collins, Aideen M. Sullivan, and Gerard W. O’Keeffe. "Gene Co-expression Analysis of the Human Substantia Nigra Identifies ZNHIT1 as an SNCA Co-expressed Gene that Protects Against α-Synuclein-Induced Impairments in Neurite Growth and Mitochondrial Dysfunction in SH-SY5Y Cells." Molecular Neurobiology 59, no. 5 (February 17, 2022): 2745–57. http://dx.doi.org/10.1007/s12035-022-02768-9.
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AbstractParkinson’s disease (PD) is neurodegenerative disorder with the pathological hallmarks of progressive degeneration of midbrain dopaminergic neurons from the substantia nigra (SN), and accumulation and spread of inclusions of aggregated α-synuclein (α-Syn). Since current PD therapies do not prevent neurodegeneration, there is a need to identify therapeutic targets that can prevent α-Syn-induced reductions in neuronal survival and neurite growth. We hypothesised that genes that are normally co-expressed with the α-Syn gene (SNCA), and whose co-expression pattern is lost in PD, may be important for protecting against α-Syn-induced dopaminergic degeneration, since broken correlations can be used as an index of functional misregulation. Gene co-expression analysis of the human SN showed that nuclear zinc finger HIT-type containing 1 (ZNHIT1) is co-expressed with SNCA and that this co-expression pattern is lost in PD. Overexpression of ZNHIT1 was found to increase deposition of the H2A.Z histone variant in SH-SY5Y cells, to promote neurite growth and to prevent α-Syn-induced reductions in neurite growth and cell viability. Analysis of ZNHIT1 co-expressed genes showed significant enrichment in genes associated with mitochondrial function. In agreement, bioenergetic state analysis of mitochondrial function revealed that ZNHIT1 increased cellular ATP synthesis. Furthermore, α-Syn-induced impairments in basal respiration, maximal respiration and spare respiratory capacity were not seen in ZNHIT1-overexpressing cells. These data show that ZNHIT1 can protect against α-Syn-induced degeneration and mitochondrial dysfunction, which rationalises further investigation of ZNHIT1 as a therapeutic target for PD.
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Mathian, Alexis, Suzanne Mouries-Martin, Karim Dorgham, Hervé Devilliers, Hans Yssel, Laura Garrido Castillo, Fleur Cohen-Aubart, et al. "Ultrasensitive serum interferon-α quantification during SLE remission identifies patients at risk for relapse." Annals of the Rheumatic Diseases 78, no. 12 (September 30, 2019): 1669–76. http://dx.doi.org/10.1136/annrheumdis-2019-215571.
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ObjectivesMaintenance of remission has become central in the management of systemic lupus erythematosus (SLE). The importance of interferon-alpha (IFN-α) in the pathogenesis of SLE notwithstanding, its expression in remission has been poorly studied as yet. To study its expression in remission and its prognostic value in the prediction of a disease relapse, serum IFN-α levels were determined using an ultrasensitive single-molecule array digital immunoassay which enables the measurement of cytokines at physiological concentrations.MethodsA total of 254 SLE patients in remission, according to the Definition of Remission in SLE classification, were included in the study. Serum IFN-α concentrations were determined at baseline and patients were followed up for 1 year. Lupus flares were defined according to the Safety of Estrogens in Lupus Erythematosus: National Assessment version of the Systemic Lupus Erythematosus Disease Activity Index Flare Index, whereas the Kaplan-Meier analysis and Cox regression analysis were used to estimate the time to relapse and to identify baseline factors associated with time to relapse, respectively.ResultsOf all patients in remission, 26% displayed abnormally high IFN-α serum levels that were associated with the presence of antibodies specific for ribonucleoprotein (RNP), double stranded (ds)DNA and Ro/SSA60, as well as young age. Importantly, elevated-baseline IFN-α serum levels and remission duration were associated in an independent fashion, with shorter time to relapse, while low serum levels of complement component 3 and anti-dsDNA Abs were not.ConclusionDirect serum IFN-α assessment with highly sensitive digital immunoassay permits clinicians to identify a subgroup of SLE patients, clinically in remission, but at higher risk of relapse.
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Wang, Linna, Jiwei Ma, Cunxia Guo, Changyong Chen, Zhong Yin, Xueguang Zhang, and Xiangmei Chen. "Danggui Buxue Tang Attenuates Tubulointerstitial Fibrosis via Suppressing NLRP3 Inflammasome in a Rat Model of Unilateral Ureteral Obstruction." BioMed Research International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9368483.
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Inflammation significantly contributes to the progression of chronic kidney disease (CKD). This study aimed to characterize Danggui Buxue Tang (DBT) renoprotection and relationship with NOD-like receptors family pyrin domain-containing 3 (NLRP3) inflammasome expression in rats with unilateral ureteral obstruction (UUO). Sprague-Dawley rats were subjected to UUO and randomly assigned to untreated UUO, enalapril-treated (10 mg/kg/day), and DBT-treated (9 g/kg/day) groups. Sham-operated rats served as controls, with 8 rats in each group. All rats were sacrificed for blood and renal specimen collection at 14 days after UUO. Untreated UUO rats exhibited azotemia, intense tubulointerstitial collagen deposition, upregulations of tubulointerstitial injury index, augmentation levels of collagen I (Col I), α-smooth muscle actin (α-SMA), NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), pro-caspase-1, caspase-1, IL-1β, and pro-IL-1β. DBT treatment significantly attenuated interstitial collagen deposition and tubulointerstitial injury, lowering Col I and α-SMA levels. Synchronous expressions of NLRP3, ASC, pro-caspase-1, caspase-1, pro-IL-1β, and IL-1β decreased in renal tissue. In comparison to enalapril, DBT significantly reduced tubulointerstitial injury, interstitial collagen deposition, and expressions of Col I and IL-1β. Thus, DBT offers renoprotection in UUO rats, which was associated with suppressing NLRP3 inflammasome expression and following reduction of the secretion of cytokine IL-1β. The mechanisms of multitargets of traditional Chinese medicine can be better used for antifibrotic treatment.
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Zhang, Mingjuan, Huaming Deng, Xiajun Yi, Siying Xie, and Qingying Zhan. "Study on Chlorogenic Acid Inhibiting the Proliferation and Invasion of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis Model." Journal of Biomaterials and Tissue Engineering 11, no. 11 (November 1, 2021): 2192–96. http://dx.doi.org/10.1166/jbt.2021.2797.
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This paper explored Chlorogenic acid regulating the biological behavior of RA FLSs and studied the functional role of microRNAs in it. In vivo experiment: Female DBA/1 J mice were used for model establishment and grouping. HE staining was employed. The damage of ankle cartilage was analyzed in each group of mice. The levels of serum cytokines TNF-α and IL-β were measured by ELISA. In vitro experiment: The cells were counterstained with Hoechst 33342, Transwell was used to detect cell invasion. Western blotting was used to detect the expression of Akt protein. The Akt expression plasmid and miR-23b mimic were co-transfected into RA FLSs, and the luciferase activity was measured using a dual-luciferase detection system. In vivo experiments found that Chlorogenic acid can significantly reduce arthritis index and inhibit TNF-α and IL-β levels. In vitro experiments found that TNF-α-induced proliferation of RA FLSs was significantly inhibited by Chlorogenic acid. Transwell invasion test showed that TNF-α-induced cell invasion was attenuated at the presence of Chlorogenic acid, which significantly inhibited Akt protein expression and phosphorylation. The expression of miR-23b in Chlorogenic acid-treated RA-FLSs increased, and silencing miR-23b enhanced the inhibitory effect of RA FLSs on Chlorogenic acid induction. Chlorogenic acid has potential anti-rheumatoid arthritis activity. Its inhibition of RA FLSs proliferation and invasion is related to the induction of miR-23b and the down-regulation of Akt expression.
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Chang, Sue-Ling, André Tchernof, Francine Durocher, and Caroline Diorio. "Associations of Biomarkers of Inflammation and Breast Cancer in the Breast Adipose Tissue of Women with Combined Measures of Adiposity." Journal of Obesity 2021 (August 13, 2021): 1–10. http://dx.doi.org/10.1155/2021/3620147.
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Background. Mechanisms underlying the obesity-breast cancer link involve inflammation but need to be elucidated. Determining obesity by combining body mass index (BMI) with the waist circumference (WC) may clarify the role of inflammatory and hormonally related markers in breast cancer. We examined the effect of combining adiposity indices (BMI/WC) with the gene expression of several biomarkers involved in breast cancer. Methods. Expression of cytochrome P450 family 19 subfamily A member 1 (CYP19A1), estrogen receptor-alpha (ER-α), allograft inflammatory factor 1 (AIF1), cyclooxygenase-2 (COX2), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and leptin (LEP) in 141 adipose breast tissues was quantified using qPCR method. BMI and WC were measured by a trained nurse and categorized using the median split, BMILOWCLO, BMILOWCHI, BMIHIWCLO, and BMIHIWCHI. Results. Gene expression of IL-6 (3-fold), TNF-α (2-fold), and LEP (2-fold) was higher in the breast adipose tissue of women with high WC regardless of BMI, that is, BMILOWCHI and BMIHIWCHI women (all P < 0.01). Compared to BMILOWCLO women, gene expression of CYP19A1, COX2, and AIF1 was increased by two-fold in breast adipose tissue of BMIHIWCHI women ( P < 0.10). ER-α was not different across adiposity categories. Conclusions. The expression of some biomarkers, particularly those related to inflammation, is elevated in breast adipose tissue of women with a high WC independent of BMI. Obesity monitoring should also include women with normal or low BMI, but with central adiposity.
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Haluzik, M. M., Z. Lacinova, M. Dolinkova, D. Haluzikova, D. Housa, A. Horinek, Z. Vernerova, T. Kumstyrova, and M. Haluzik. "Improvement of Insulin Sensitivity after Peroxisome Proliferator-Activated Receptor-α Agonist Treatment Is Accompanied by Paradoxical Increase of Circulating Resistin Levels." Endocrinology 147, no. 9 (September 1, 2006): 4517–24. http://dx.doi.org/10.1210/en.2005-1624.
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We studied the effect of peroxisome proliferator-activated receptor-α (PPAR-α) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-α agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-α activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.
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Lucini, Daniela, Massimo Pagani, Giuseppe Sandro Mela, and Alberto Malliani. "Sympathetic Restraint of Baroreflex Control of Heart Period in Normotensive and Hypertensive Subjects." Clinical Science 86, no. 5 (May 1, 1994): 547–56. http://dx.doi.org/10.1042/cs0860547.
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1. We assessed the effects of changing levels of sympathetic drive on the gain of baroreflex control of the sino-atrial node, in normotensive and hypertensive subjects. 2. Autoregressive spectral and cross-spectral analysis of R—R interval and systolic arterial pressure (non-invasive Finapres method) variabilities providing an estimate of baroreflex gain through the frequency domain index α were performed on data from 63 normotensive and 78 mild hypertensive subjects. Subjects were studied at rest and during active orthostatism, which induces sympathetic predominance. Seven control subjects and 14 hypertensive subjects were also studied after chronic atenolol treatment, to attenuate β-adrenoceptor-mediated responses. 3. In both normotensive and hypertensive subjects, the index α was reduced by active standing and increased by chronic β-adrenoceptor blockade. Furthermore, at rest, the index at was correlated with R—R variance and appeared significantly reduced with age. The age-related negative correlation of the index α was no longer evident during the standing-induced increase in sympathetic drive, in both normotensive and hypertensive subjects. 4. The index α, a non-invasive frequency domain estimate of the overall gain of baroreflex control of the sino-atrial node, which appears to be reduced in essential hypertension, is negatively modulated by physiological increases in sympathetic drive, and augmented by pharmacological blockade of β-adrenoceptors. 5. In essential hypertension the enhanced sympathetic drive present already at rest, and the simultaneous reduction of the gain of baroreflex mechanisms, are the expression of a complex alteration in neural cardiovascular control.
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Arellano-Buendía, Abraham Said, Luis Gerardo Castañeda-Lara, María L. Loredo-Mendoza, Fernando E. García-Arroyo, Pedro Rojas-Morales, Raúl Argüello-García, Juan G. Juárez-Rojas, et al. "Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes." Antioxidants 9, no. 11 (November 15, 2020): 1134. http://dx.doi.org/10.3390/antiox9111134.
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This study aimed to assess the impact of allicin on the course of diabetic nephropathy. Study groups included control, diabetes, and diabetes-treated rats. Allicin treatment (16 mg/kg day/p.o.) started after 1 month of diabetes onset and was administered for 30 days. In the diabetes group, the systolic blood pressure (SBP) increased, also, the oxidative stress and hypoxia in the kidney cortex were evidenced by alterations in the total antioxidant capacity as well as the expression of nuclear factor (erythroid-derived 2)-like 2/Kelch ECH associating protein 1 (Nrf2/Keap1), hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), erythropoietin (Epo) and its receptor (Epo-R). Moreover, diabetes increased nephrin, and kidney injury molecule-1 (KIM-1) expression that correlated with mesangial matrix, the fibrosis index and with the expression of connective tissue growth factor (CTGF), transforming growth factor-β1 (TGF-β1), and α-smooth muscle actin (α-SMA). The insulin levels and glucose transporter protein type-4 (GLUT4) expression were decreased; otherwise, insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) expression was increased. Allicin increased Nrf2 expression and decreased SBP, Keap1, HIF-1α, and VEGF expression. Concurrently, nephrin, KIM-1, the mesangial matrix, fibrosis index, and the fibrotic proteins were decreased. Additionally, allicin decreased hyperglycemia, improved insulin levels, and prevented changes in (GLUT4) and IRSs expression induced by diabetes. In conclusion, our results demonstrate that allicin has the potential to help in the treatment of diabetic nephropathy. The cellular mechanisms underlying its effects mainly rely on the regulation of antioxidant, antifibrotic, and antidiabetic mechanisms, which can contribute towards delay in the progression of renal disease.
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Palau, Vanesa, Josué Jarrín, Sofia Villanueva, David Benito, Eva Márquez, Eva Rodríguez, María José Soler, et al. "Endothelial ADAM17 Expression in the Progression of Kidney Injury in an Obese Mouse Model of Pre-Diabetes." International Journal of Molecular Sciences 23, no. 1 (December 25, 2021): 221. http://dx.doi.org/10.3390/ijms23010221.
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Disintegrin and metalloproteinase domain 17 (ADAM17) activates inflammatory and fibrotic processes through the shedding of various molecules such as Tumor Necrosis Factor-α (TNF-α) or Transforming Growht Factor-α (TGF-α). There is a well-recognised link between TNF-α, obesity, inflammation, and diabetes. In physiological situations, ADAM17 is expressed mainly in the distal tubular cell while, in renal damage, its expression increases throughout the kidney including the endothelium. The aim of this study was to characterize, for the first time, an experimental mouse model fed a high-fat diet (HFD) with a specific deletion of Adam17 in endothelial cells and to analyse the effects on different renal structures. Endothelial Adam17 knockout male mice and their controls were fed a high-fat diet, to induce obesity, or standard rodent chow, for 22 weeks. Glucose tolerance, urinary albumin-to-creatinine ratio, renal histology, macrophage infiltration, and galectin-3 levels were evaluated. Results showed that obese mice presented higher blood glucose levels, dysregulated glucose homeostasis, and higher body weight compared to control mice. In addition, obese wild-type mice presented an increased albumin-to-creatinine ratio; greater glomerular size and mesangial matrix expansion; and tubular fibrosis with increased galectin-3 expression. Adam17 deletion decreased the albumin-to-creatinine ratio, glomerular mesangial index, and tubular galectin-3 expression. Moreover, macrophage infiltration in the glomeruli of obese Adam17 knockout mice was reduced as compared to obese wild-type mice. In conclusion, the expression of ADAM17 in endothelial cells impacted renal inflammation, modulating the renal function and histology in an obese pre-diabetic mouse model.
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El Midaoui, Adil, Calin Lungu, Hui Wang, Lingyun Wu, Caroline Robillard, Denis DeBlois, and Réjean Couture. "Impact of α-lipoic acid on liver peroxisome proliferator-activated receptor-α, vascular remodeling, and oxidative stress in insulin-resistant rats." Canadian Journal of Physiology and Pharmacology 89, no. 10 (October 2011): 743–51. http://dx.doi.org/10.1139/y11-072.
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This study sought to determine the impact of α-lipoic acid (LA) on superoxide anion (O2•–) production and peroxisome proliferator-activated receptor-α (PPARα) expression in liver tissue, plasma free fatty acids (FFA), and aortic remodeling in a rat model of insulin resistance. Sprague–Dawley rats (50–75 g) were given either tap water or a drinking solution containing 10% D-glucose for 14 weeks, combined with a diet with or without LA supplement. O2•– production was measured by lucigenin chemiluminescence, and PPAR-α expression by Western blotting. Cross-sectional area (CSA) of the aortic media and lumen and number of smooth muscle cells (SMC) were determined histologically. Glucose increased systolic blood pressure (SBP), plasma levels of glucose and insulin, and insulin resistance (HOMA index). All of these effects were attenuated by LA. Whereas glucose had no effect on liver PPAR-α protein level, it decreased plasma FFA. LA decreased the aortic and liver O2•– production, body weight, and plasma FFA levels in control and glucose-treated rats. Liver PPAR-α protein levels were increased by LA, and negatively correlated with plasma FFA. Medial CSA was reduced in all glucose-treated rats, and positively correlated with plasma FFA but not with SBP or aortic O2•– production. Glucose also reduced aortic lumen area, so that the media-to-lumen ratio remained unchanged. The ability of LA to lower plasma FFA appears to be mediated, in part, by increased hepatic PPAR-α expression, which may positively affect insulin resistance. Glucose-fed rats may serve as a unique model of aortic atrophic remodeling in hypertension and early metabolic syndrome.
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Tisato, Veronica, Paola Secchiero, Erika Rimondi, Sergio Gianesini, Erica Menegatti, Fabio Casciano, Paolo Zamboni, and Giorgio Zauli. "GM-CSF Exhibits Anti-Inflammatory Activity on Endothelial Cells Derived from Chronic Venous Disease Patients." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/561689.
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Twenty patients affected by chronic venous disease (CVD) in tertiary venous network and/or saphenous vein were analyzed before surgical ablation by echo-color-doppler for the hemodynamic parameters reflux time (RT) and resistance index (RI), a negative and a positive prognostic factor, respectively. RT and RI were next correlated with relevantin vitroparameters of venous endothelial cells (VEC) obtained from surgical specimens, such as cell migration in response to serum gradient, proliferation index, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression, as well as cytokines release. Of interest, ICAM-1 expression in patient-derived VEC cultures correlated positively with RT and negatively with RI. Moreover, RT showed a positive correlation with the baseline osteoprotegerin (OPG) expression by VEC and an inverse correlation with VEC proliferation index. On the other hand, RI correlated positively with TNF-related apoptosis inducing ligand (TRAIL) expression. Among the cytokines released by VEC, GM-CSF showed a positive correlation with VEC proliferation and TRAIL expression and a negative correlation with OPG, ICAM-1 and VCAM-1 expression. Sincein vitrorecombinant GM-CSF induced VEC proliferation and counteracted the induction of ICAM-1, VCAM-1 and OPG upon exposure to TNF-α, our data suggest an anti-inflammatory activity of GM-CSF on venous endothelial cells.
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Wang, Ya-Yu, Shih-Yi Lin, Yu-Han Chuang, Wayne Huey-Herng Sheu, Kwong-Chung Tung, and Chun-Jung Chen. "Activation of Hepatic Inflammatory Pathways by Catecholamines Is Associated With Hepatic Insulin Resistance in Male Ischemic Stroke Rats." Endocrinology 155, no. 4 (April 1, 2014): 1235–46. http://dx.doi.org/10.1210/en.2013-1593.
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Patients who experience acute ischemic stroke may develop hyperglycemia, even in the absence of diabetes. In the current study we determined the effects of acute stroke on hepatic insulin signaling, TNF-α expression, endoplasmic reticulum (ER) stress, the activities of c-Jun N-terminal kinase (JNK), inhibitor κB kinase β (IKK-β), and nuclear factor-κB (NF-κB) pathways. Rats with cerebral ischemia developed higher blood glucose, and insulin levels, and insulin resistance index, as well as hepatic gluconeogenic enzyme expression compared with the sham-treated group. The hepatic TNF-α mRNA and protein levels were elevated in stroke rats in association with increased ER stress, phosphorylation of JNK1/2 and IKK-β proteins, IκB/NF-κB signaling, and phosphorylation of insulin receptor-1 (IRS-1) at serine residue. The basal and insulin-stimulated tyrosine phosphorylation of IRS-1 and AKT proteins was reduced. In addition, acute stroke increased circulating catecholamines in association with hepatic adrenergic signaling activation. After administration of a nonselective β-adrenergic receptor blocker (propranolol) before induction of cerebral ischemic injury, hepatic adrenergic transduction, TNF-α expression, ER stress, and the activation of the JNK1/2, IKK-β, and NF-κB pathways, and serine phosphorylation of IRS-1 were all attenuated. In contrast, the phosphorylated IRS-1 at tyrosine site and AKT levels were partially restored with improved poststroke hyperglycemia and insulin resistance index. These results suggest that acute ischemic stroke can activate proinflammatory pathways in the liver by the catecholamines and is associated with the development of hepatic insulin resistance.
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Motevalian, Manijeh, Siyavash Joukar, Saeed Esmaeili-Mahani, Abdollah Karimi, Yaser Masoumi-Ardakani, and Sepideh Safari. "Interaction of high-intensity endurance exercise and nandrolone on cardiac remodeling: role of adipo-cardiac axis." Hormone Molecular Biology and Clinical Investigation 43, no. 1 (November 16, 2021): 63–70. http://dx.doi.org/10.1515/hmbci-2021-0042.
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Abstract Objectives Given the cardiac pathological remodeling following to anabolic androgenic steroids (AASs) consumption, we examined the effect of chronic administration of nandrolone decanoate with high-intensity endurance exercise on the left ventricular hypertrophy index, levels of hydroxyproline, tumor necrosis factor-alpha (TNF-α), adiponectin (APN) and its receptors (AdipoR1 and AdipoR2) expression in rats’ hearts. Methods The male Wistar rats randomly divided to six groups included the control (CTL), exercise (Ex), nandrolone (Nan), vehicle (Arach), trained vehicle (Ex + Arach), and trained nandrolone (Ex + Nan) groups that were treated for eight weeks. Results Nandrolone consumption significantly enhanced the hypertrophy index (p<0.05) and exercise intensified this effect. It also increased the level of cardiac hydroxyproline (p<0.001), however exercise completely masked this effect. The values of TNF-α protein and AdipoR1 protein significantly increased in trained nandrolone-treated (Ex + Nan) group in comparison with CTL group (p<0.05), however, did not show significant alteration in Nan or Ex groups. High-intensity endurance exercise significantly enhanced the AdipoR2 protein (p<0.05), but, co-administration of nandrolone with exercise prevented this effect. The mRNA expression of AdipoR1 significantly reduced in the animals that received nandrolone for eight weeks and exercise recovered this effect (p<0.001). Conclusions Despite an additive effect of high-intensity endurance exercise plus nandrolone on TNF-α level, their effects on hydroxyproline and APN receptors expression is incompatible in heart of rat. It is suggests a part of beneficial regulatory role of endurance exercise against nandrolone induced heart remodeling may apply through modulation of APN system.
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Castan-Laurell, Isabelle, Michaela Vítkova, Danièle Daviaud, Cédric Dray, Michaela Kováčiková, Zuzana Kovacova, Jindriska Hejnova, Vladimir Stich, and Philippe Valet. "Effect of hypocaloric diet-induced weight loss in obese women on plasma apelin and adipose tissue expression of apelin and APJ." European Journal of Endocrinology 158, no. 6 (June 2008): 905–10. http://dx.doi.org/10.1530/eje-08-0039.
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ObjectiveApelin is a novel adipokine acting on APJ receptor, regulated by insulin and tumor necrosis factor-α (TNF-α) in adipose tissue (AT). Plasma apelin levels are increased in obese hyperinsulinemic subjects. The aim was to investigate whether the hypocaloric diet associated with weight loss modifies the elevated plasma apelin levels and the expression of apelin and APJ receptor in AT in obese women.Design and methodsFasting plasma levels of apelin and TNF-α as well as mRNA levels of apelin and APJ in AT were measured before and after a 12-week hypocaloric weight-reducing diet in 20 obese women (body mass index (BMI) before diet 32.2±6.4 kg/m2). Twelve healthy women with a BMI of 20.7±0.6 kg/m2 served as reference.ResultsPlasma levels of apelin and TNF-α were higher in obese compared with lean controls. The hypocaloric diet resulted in a significant decrease of BMI to 29.8±6.3 kg/m2, plasma insulin (8.16±0.73 to 6.58±0.66 mU/l), apelin (369±25 pg/ml to 257±12 pg/ml), TNF-α levels (0.66±0.04 pg/ml to 0.56±0.04 pg/ml), and AT mRNAs of apelin and APJ. In addition, changes in AT mRNA apelin were related to changes in AT mRNA APJ levels.ConclusionThe hypocaloric diet associated with weight loss reduces the increased plasma and AT expression of apelin in obese women. This reduced apelin expression in AT could contribute to decreased circulating apelin levels.
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Petersen, Anne Marie Winther, Faidon Magkos, Philip Atherton, Anna Selby, Kenneth Smith, Michael J. Rennie, Bente Klarlund Pedersen, and Bettina Mittendorfer. "Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFbx in muscle." American Journal of Physiology-Endocrinology and Metabolism 293, no. 3 (September 2007): E843—E848. http://dx.doi.org/10.1152/ajpendo.00301.2007.
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Smoking causes multiple organ dysfunction. The effect of smoking on skeletal muscle protein metabolism is unknown. We hypothesized that the rate of skeletal muscle protein synthesis is depressed in smokers compared with non-smokers. We studied eight smokers (≥20 cigarettes/day for ≥20 years) and eight non-smokers matched for sex (4 men and 4 women per group), age (65 ± 3 and 63 ± 3 yr, respectively; means ± SEM) and body mass index (25.9 ± 0.9 and 25.1 ± 1.2 kg/m2, respectively). Each subject underwent an intravenous infusion of stable isotope-labeled leucine in conjunction with blood and muscle tissue sampling to measure the mixed muscle protein fractional synthesis rate (FSR) and whole body leucine rate of appearance (Ra) in plasma (an index of whole body proteolysis), the expression of genes involved in the regulation of muscle mass (myostatin, a muscle growth inhibitor, and MAFBx and MuRF-1, which encode E3 ubiquitin ligases in the proteasome proteolytic pathway) and that for the inflammatory cytokine TNF-α in muscle, and the concentration of inflammatory markers in plasma (C-reactive protein, TNF-α, interleukin-6) which are associated with muscle wasting in other conditions. There were no differences between nonsmokers and smokers in plasma leucine concentration, leucine rate of appearance, and plasma concentrations of inflammatory markers, or TNF-α mRNA in muscle, but muscle protein FSR was much less (0.037 ± 0.005 vs. 0.059 ± 0.005%/h, respectively, P = 0.004), and myostatin and MAFBx (but not MuRF-1) expression were much greater (by ∼33 and 45%, respectivley, P < 0.05) in the muscle of smokers than of nonsmokers. We conclude that smoking impairs the muscle protein synthesis process and increases the expression of genes associated with impaired muscle maintenance; smoking therefore likely increases the risk of sarcopenia.
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Royal, W., S. Gartner, and C. D. Gajewski. "Retinol measurements and retinoid receptor gene expression in patients with multiple sclerosis." Multiple Sclerosis Journal 8, no. 6 (December 2002): 452–58. http://dx.doi.org/10.1191/1352458502ms858oa.
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Treatment with interferon (IFN)-β1a has been associated with decreased disease activity in patients with multiple sclerosis (MS). In several biological systems, type I IFNs and retinoids have been demonstrated to have synergistic effects. In these studies, we measured blood and cerebrospinal fluid (CSF) retinol levels and naïve and memory T-helper cell subset percentages in samples from a group of patients with MS. We also examined retinol receptor expression in peripheral blood cells from MS patients with or without a history of prior treatment with IFN-β1a. The mean plasma retinol level for untreated relapsing-remitting (RR) MS patients was lower than for patients with noninflammatory neurological disease. Among IFN-β1a-treated RR patients, mean levels were slightly higher than for RR patients not on treatment. Lower plasma retinol levels among the MS patients studied were associated with higher CSF retinol index measurements - a measure that was calculated to correct for nonspecific leakage of retinol from blood into CSF. For the MS samples examined, there was a borderline statistically significant direct correlation between CSF retinol index measurements and CSF memory T-helper cell percentages. Examination of peripheral blood from untreated RR patients for retinoid receptor mRNA expression revealed the expression of the retinoic acid receptor (RAR)-α, RAR-γ, and retinoic X receptor (RXR)-α receptor subtypes. For RR patients on IFN-β1a therapy, expression of the same RAR subtypes was noted as well as expression of RXR-βand RXR-γ. These studies suggest an association between plasma retinol levels and clinical disease activity in patients with MS and that treatment with IFN-β1a may be associated with activation of specific retinoid receptor subtypes.
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Tonecka, Katarzyna, Agata Braniewska, Zofia Pilch, Zuzanna Sas, Marcin Skorzynski, Elisabetta Manuali, and Tomasz P. Rygiel. "The CD200 Regulates Inflammation in Mice Independently of TNF-α Production." International Journal of Molecular Sciences 22, no. 10 (May 19, 2021): 5358. http://dx.doi.org/10.3390/ijms22105358.
Full textAbstract:
Inflammatory bowel disease is characterized by the infiltration of immune cells and chronic inflammation. The immune inhibitory receptor, CD200R, is involved in the downregulation of the activation of immune cells to prevent excessive inflammation. We aimed to define the role of CD200R ligand-CD200 in the experimental model of intestinal inflammation in conventionally-reared mice. Mice were given a dextran sodium sulfate solution in drinking water. Bodyweight loss was monitored daily and the disease activity index was calculated, and a histological evaluation of the colon was performed. TNF-α production was measured in the culture of small fragments of the distal colon or bone marrow-derived macrophages (BMDMs) cocultured with CD200+ cells. We found that Cd200−/− mice displayed diminished severity of colitis when compared to WT mice. Inflammation significantly diminished CD200 expression in WT mice, particularly on vascular endothelial cells and immune cells. The co-culture of BMDMs with CD200+ cells inhibited TNF-α secretion. In vivo, acute colitis induced by DSS significantly increased TNF-α secretion in colon tissue in comparison to untreated controls. However, Cd200−/− mice secreted a similar level of TNF-α to WT mice in vivo. CD200 regulates the severity of DSS-induced colitis in conventionally-reared mice. The presence of CD200+ cells decreases TNF-α production by macrophages in vitro. However, during DDS-induced intestinal inflammation secretion of TNF-α is independent of CD200 expression.
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Cejka, Cestmir, Vladimir Holan, Peter Trosan, Alena Zajicova, Eliska Javorkova, and Jitka Cejkova. "The Favorable Effect of Mesenchymal Stem Cell Treatment on the Antioxidant Protective Mechanism in the Corneal Epithelium and Renewal of Corneal Optical Properties Changed after Alkali Burns." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/5843809.
Full textAbstract:
The aim of this study was to examine whether mesenchymal stem cells (MSCs) and/or corneal limbal epithelial stem cells (LSCs) influence restoration of an antioxidant protective mechanism in the corneal epithelium and renewal of corneal optical properties changed after alkali burns. The injured rabbit corneas (with 0.25 N NaOH) were untreated or treated with nanofiber scaffolds free of stem cells, with nanofiber scaffolds seeded with bone marrow MSCs (BM-MSCs), with adipose tissue MSCs (Ad-MSCs), or with LSCs. On day 15 following the injury, after BM-MSCs or LSCs nanofiber treatment (less after Ad-MSCs treatment) the expression of antioxidant enzymes was restored in the regenerated corneal epithelium and the expressions of matrix metalloproteinase 9 (MMP9), inducible nitric oxide synthase (iNOS), α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and vascular endothelial factor (VEGF) were low. The central corneal thickness (taken as an index of corneal hydration) increased after the injury and returned to levels before the injury. In injured untreated corneas the epithelium was absent and numerous cells revealed the expressions of iNOS, MMP9, α-SMA, TGF-β1, and VEGF. In conclusion, stem cell treatment accelerated regeneration of the corneal epithelium, restored the antioxidant protective mechanism, and renewed corneal optical properties.