Relevant bibliographies by topics / MicroRNA, Neutrophils, RNAsequencing, Apoptosis

Academic literature on the topic 'MicroRNA, Neutrophils, RNAsequencing, Apoptosis'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "MicroRNA, Neutrophils, RNAsequencing, Apoptosis"

1

Xue, H., and MX Li. "MicroRNA-150 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation." Human & Experimental Toxicology 37, no. 9 (December 5, 2017): 920–28. http://dx.doi.org/10.1177/0960327117741749.

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Cigarette smoke (CS) exposure is an important risk factor for chronic obstructive pulmonary disease (COPD). MicroRNA-150 (miR-150) is involved in several inflammatory diseases. However, little is known about the role of miR-150 in the pathogenesis of COPD. In this study, we established a CS-related mouse model of COPD and evaluated the impact of miR-150 on CS-induced lung inflammation. We further investigated the effects of miR-150 overexpression on pro-inflammatory cytokine production and apoptosis in airway epithelial cells exposed to CS extract (CSE). It was found that miR-150 was significantly ( p < 0.05) downregulated in the lungs of CS-exposed mice, compared to control mice under normal air. The CSE-exposed BEAS-2B airway epithelial cells displayed a four- to six-fold reduction in miR-150 levels, compared to control cells ( p < 0.05). Delivery of miR-150 mimic attenuated CS-induced lung inflammation and accumulation of neutrophils, lymphocytes, and macrophages in bronchoalveolar lavage fluid. Moreover, miR-150 overexpression prevented the induction of interleukin-6, tumor necrosis factor alpha, and interleukin-8 expression and nuclear factor kappa B (NF-κB) transcriptional activity in BEAS-2B cells by CSE. Additionally, miR-150 protected BEAS-2B cells from CSE-induced apoptosis, which was associated with reduced p53 expression. Co-expression of p53 restored apoptotic response to CSE in miR-150-overexpressing BEAS-2B cells. Collectively, miR-150 suppresses CS-induced lung inflammation and airway epithelial cell apoptosis, which is causally linked to repression of p53 expression and NF-κB activity. Restoration of miR-150 expression may represent a potential therapeutic strategy for CS-related COPD.
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Hutcheson, Rebecca, Russell Terry, Brenda Hutcheson, Rashmi Jadhav, Jennifer Chaplin, Erika Smith, Robert Barrington, Spencer D. Proctor, and Petra Rocic. "miR-21-mediated decreased neutrophil apoptosis is a determinant of impaired coronary collateral growth in metabolic syndrome." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 11 (June 1, 2015): H1323—H1335. http://dx.doi.org/10.1152/ajpheart.00654.2014.

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Coronary collateral growth (CCG) is impaired in metabolic syndrome. microRNA-21 (miR-21) is a proproliferative and antiapoptotic miR, which we showed to be elevated in metabolic syndrome. Here we investigate whether impaired CCG in metabolic syndrome involved miR-21-mediated aberrant apoptosis. Normal Sprague-Dawley (SD) and metabolic syndrome [J. C. Russel (JCR)] rats underwent transient, repetitive coronary artery occlusion [repetitive ischemia (RI)]. Antiapoptotic Bcl-2, phospho-Bad, and Bcl-2/Bax dimers were increased on days 6 and 9 RI, and proapoptotic Bax and Bax/Bax dimers and cytochrome- c release concurrently decreased in JCR versus SD rats. Active caspases were decreased in JCR versus SD rats (∼50%). Neutrophils increased transiently on day 3 RI in the collateral-dependent zone of SD rats but remained elevated in JCR rats, paralleling miR-21 expression. miR-21 downregulation by anti-miR-21 induced neutrophil apoptosis and decreased Bcl-2 and Bcl-2/Bax dimers (∼75%) while increasing Bax/Bax dimers, cytochrome- c release, and caspase activation (∼70, 400, and 400%). Anti-miR-21 also improved CCG in JCR rats (∼60%). Preventing neutrophil infiltration with blocking antibodies resulted in equivalent CCG recovery, confirming a major role for deregulated neutrophil apoptosis in CCG impairment. Neutrophil and miR-21-dependent CCG inhibition was in significant part mediated by increased oxidative stress. We conclude that neutrophil apoptosis is integral to normal CCG and that inappropriate prolonged miR-21-mediated survival of neutrophils plays a major role in impaired CCG, in part via oxidative stress generation.
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Velázquez, Kandy T., Reilly T. Enos, Jamie L. McClellan, Taryn L. Cranford, Ioulia Chatzistamou, Udai P. Singh, Mitzi Nagarkatti, Prakash S. Nagarkatti, Daping Fan, and E. Angela Murphy. "MicroRNA-155 deletion promotes tumorigenesis in the azoxymethane-dextran sulfate sodium model of colon cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 6 (March 15, 2016): G347—G358. http://dx.doi.org/10.1152/ajpgi.00326.2015.

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Clinical studies have linked microRNA-155 (miR-155) expression in the tumor microenvironment to poor prognosis. However, whether miR-155 upregulation is predictive of a pro- or antitumorigenic response is unclear, as the limited preclinical data available remain controversial. We examined miR-155 expression in tumor tissue from colon cancer patients. Furthermore, we investigated the role of this microRNA in proliferation and apoptosis, inflammatory processes, immune cell populations, and transforming growth factor-β/SMAD signaling in a chemically induced (azoxymethane-dextran sulfate sodium) mouse model of colitis-associated colon cancer. We found a higher expression of miR-155 in the tumor region than in nontumor colon tissue of patients with colon cancer. Deletion of miR-155 in mice resulted in a greater number of polyps/adenomas, an increased symptom severity score, a higher grade of epithelial dysplasia, and a decrease in survival. Surprisingly, these findings were associated with an increase in apoptosis in the normal mucosa, but there was no change in proliferation. The protumorigenic effects of miR-155 deletion do not appear to be driven solely by dysregulation of inflammation, as both genotypes had relatively similar levels of inflammatory mediators. The enhanced tumorigenic response in miR-155−/− mice was associated with alterations in macrophages and neutrophils, as markers for these populations were decreased and increased, respectively. Furthermore, we demonstrated a greater activation of the transforming growth factor-β/SMAD pathway in miR-155−/− mice, which was correlated with the increased tumorigenesis. Given the multiple targets of miR-155, careful evaluation of its role in tumorigenesis is necessary prior to any consideration of its potential as a biomarker and/or therapeutic target in colon cancer.
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Ma, Xiaoqing, Ho Jun Yun, Kenneth Elkin, Yunliang Guo, Yuchuan Ding, and Guangwen Li. "MicroRNA-29b Suppresses Inflammation and Protects Blood-Brain Barrier Integrity in Ischemic Stroke." Mediators of Inflammation 2022 (August 23, 2022): 1–11. http://dx.doi.org/10.1155/2022/1755416.

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Objectives. Following cerebral ischemia, microRNA- (miR-) 29b in circulating blood is downregulated. This study investigates the underlying mechanism and implications of miR-29b in leukocyte induction. Methods. miR-29b from stroke patients and rats with middle cerebral artery occlusion (MCAO) were assessed using real-time polymerase chain reaction (PCR). miR-29b agomir was used to increase miR-29b expression in leukocytes via intravenous injection. C1q and tumor necrosis factor (C1QTNF) 6, interleukin- (IL-) 1β, zonula occludens- (ZO-) 1, occludin, and ischemic outcomes were assessed in MCAO rats. Additionally, hCMEC/D3 cells were subjected to oxygen–glucose deprivation (OGD) and cocultured with HL-60 cells. Results. miR-29b levels in neutrophils were found to be significantly lower in stroke patients compared with healthy controls, which may indicate its high diagnostic sensitivity and specificity for stroke. Moreover, miR-29b levels in leukocytes showed a negative correlation with National Institute of Health Stroke Scale (NIHSS) scores and C1QTNF6 levels. In MCAO rats, miR-29b overexpression reduced brain infarct volume and brain edema, decreasing IL-1β levels in leukocytes and in the brain 24 hours poststroke. miR-29b attenuated IL-1β expression via C1QTNF6 inhibition, leading to decreased blood-brain barrier (BBB) disruption and leukocyte infiltration. Moreover, miR-29b overexpression in HL-60 cells downregulated OGD-induced hCMEC/D3 cell apoptosis and increased ZO-1 and occludin levels in vitro. Conclusion. Leukocytic miR-29b attenuates inflammatory response by augmenting BBB integrity through C1QTNF6, suggesting a novel miR-29b-based therapeutic therapy for ischemic stroke.
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Ling, Lan, Hai-Tao Lu, Hai-Feng Wang, Mei-Jia Shen, and Hong-Bo Zhang. "MicroRNA-203 Acts as a Potent Suppressor in Septic Shock by Alleviating Lung Injury via Inhibition of VNN1." Kidney and Blood Pressure Research 44, no. 4 (2019): 565–82. http://dx.doi.org/10.1159/000500484.

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Background: Septic shock, the most serious complication of sepsis, is a life-threatening disease that is mainly characterized by hypoperfusion and multiple organ failure. Various aberrantly expressed microRNAs (miRNAs) have been reported to be related to septic shock. We explored the regulatory effect of microRNA-203 (miR-203) on lung injury in septic shock mice. Methods: Microarray-based gene expression profiling related to septic shock identified the differentially expressed gene vanin-1 (VNN1) and potential regulatory miR-203. miR-203 was predicted to mediate VNN1 expression, thus affecting septic shock, which was investigated by treatment with miR-203 mimic, miR-203 inhibitor, and siRNA-VNN1 in septic shock mouse models. Polymorphonuclear neutrophils (PMNs) and pulmonary alveolar macrophages in bronchoalveolar lavage fluid (BALF) as well as the wet/dry ratio of the lung were also measured to assess lung injury. Additionally, the effects of miR-203 on inflammatory cytokines, oxidative stress indexes, blood biochemical indexes, serine-threonine protein kinase (AKT) signaling pathway-related factors, and apoptosis-related factors were determined. Results: VNN1 was verified to be targeted and negatively regulated by miR-203. In mouse models of septic shock, weak expression of miR-203, high expression of VNN1, and inhibition of AKT signaling pathway were identified. In response to miR-203 mimic and VNN1 gene silencing, mouse models of septic shock displayed reduced apoptosis, MDA, ALT, and AST in lung tissues, decreased levels of TNF-α, IL-1β, IFN-γ, IL-10, and IL-6, in serum, and reduced PMN and PAM levels in BALF, in addition to elevated SOD activity. Notably, the presence of miR-203 mimic led to AKT signaling pathway activation. Conclusion:This study shows that upregulating miR-203 can alleviate lung injury through activation of the AKT signaling pathway by downregulating VNN1 in septic shock.
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Joseph, Gregory, Amanda Soler, Rebecca Hutcheson, Ian Hunter, Chastity Bradford, Brenda Hutcheson, Katherine H. Gotlinger, et al. "Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 3 (March 1, 2017): H528—H540. http://dx.doi.org/10.1152/ajpheart.00561.2016.

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Coronary collateral growth (CCG) is impaired in metabolic syndrome (MetS). microRNA-145 (miR-145-Adv) delivery to our rat model of MetS (JCR) completely restored and neutrophil depletion significantly improved CCG. We determined whether low endogenous levels of miR-145 in MetS allowed for elevated production of 20-hydroxyeicosatetraenoic acid (20-HETE), which, in turn, resulted in excessive neutrophil accumulation and endothelial dysfunction leading to impaired CCG. Rats underwent 0–9 days of repetitive ischemia (RI). RI-induced cardiac CYP4F (neutrophil-specific 20-HETE synthase) expression and 20-HETE levels were increased (4-fold) in JCR vs. normal rats. miR-145-Adv and 20-HETE antagonists abolished and neutrophil depletion (blocking antibodies) reduced (~60%) RI-induced increases in CYP4F expression and 20-HETE production in JCR rats. Impaired CCG in JCR rats (collateral-dependent blood flow using microspheres) was completely restored by 20-HETE antagonists [collateral-dependent zone (CZ)/normal zone (NZ) flow ratio was 0.76 ± 0.07 in JCR + 20-SOLA, 0.84 ± 0.05 in JCR + 20-HEDGE vs. 0.11 ± 0.02 in JCR vs. 0.84 ± 0.03 in normal rats]. In JCR rats, elevated 20-HETE was associated with excessive expression of endothelial adhesion molecules and neutrophil infiltration, which were reversed by miR-145-Adv. Endothelium-dependent vasodilation of coronary arteries, endothelial nitric oxide synthase (eNOS) Ser1179 phosphorylation, eNOS-dependent NO·− production and endothelial cell survival were compromised in JCR rats. These parameters of endothelial dysfunction were completely reversed by 20-HETE antagonism or miR-145-Adv delivery, whereas neutrophil depletion resulted in partial reversal (~70%). We conclude that low miR-145 in MetS allows for increased 20-HETE, mainly from neutrophils, which compromises endothelial cell survival and function leading to impaired CCG. 20-HETE antagonists could provide viable therapy for restoration of CCG in MetS. NEW & NOTEWORTHY Elevated 20-hydroxyeicosatetraenoic acid (20-HETE) impairs coronary collateral growth (CCG) in metabolic syndrome by eliciting endothelial dysfunction and apoptosis via excessive neutrophil infiltration. 20-HETE antagonists completely restore coronary collateral growth in metabolic syndrome. microRNA-145 (miR-145) is an upstream regulator of 20-HETE production in metabolic syndrome; low expression of miR-145 in metabolic syndrome promotes elevated production of 20-HETE.
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7

Shikama, Yayoi, Meiwan Cao, Tomoyuki Ono, Michiko Anzai, Hideyoshi Noji, Xiaomin Feng, Hideo Kimura, et al. "Excessive TNF-α Production Results from Reduction of c-Fos Via Aberrant Expression of Mir-34a in Neutrophils from Myelodysplastic Syndrome Patients." Blood 126, no. 23 (December 3, 2015): 1650. http://dx.doi.org/10.1182/blood.v126.23.1650.1650.

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Abstract The molecular basis of ineffective hematopoiesis in myelodysplastic syndromes (MDS) has yet to be defined. Elevation of tumor necrosis factor (TNF)-α in bone marrow plasma has been considered to be a cause of apoptosis of hematopoietic progenitor cells, and this could result in ineffective hematopoiesis in MDS. However, the mechanism of TNF-α elevation has not been elucidated. We recently found aberrant regulation of c-fos mRNA stability in neutrophils isolated from MDS patients (Feng et al, PLoS ONE, 2013). Since the expression levels of RNA-binding proteins that regulated c-fos mRNA stability were not altered in the majority of the patients and no mutations were detected in c-fos mRNA, microRNAs were possibly involved in the insufficient stabilization of c-fos mRNA. In this study, we chose 20 microRNAs targeting c-fos according to four different databases and compared their expression levels in neutrophils between MDS patients and healthy volunteers. Among them, miR-34a and miR-155 were significantly increased in MDS (p<0.05, p<0.05). Aberrantly high expressions of miR-34a and miR-155, which were defined as greater levels than the average in the healthy cells plus 2 standard deviations, were respectively detected in 14 and 13 out of 23 patients with RCUD, RCMD, and RAEB-1. We next examined the effects of the microRNA overexpression on c-fos expression. When miR-34a and miR-155 were introduced into HL60 cells by electroporation to increase their levels to 100-fold or higher than those in the control cells, c-fos protein levels decreased to 35.0 ± 10.9% and 47.8 ± 6.8% of that in the control cells, respectively, while mRNA was not altered. In neutrophils from the patients, c-fos protein but not mRNA was significantly decreased in 13 out of 17 patients tested. The c-fos protein levels were inversely correlated with miR-34a levels (r = -0.618, p<0.05) but not with those of miR-155 (r = -0.135), suggesting that c-fos protein levels were more affected by miR-34a than miR-155. Recently, it was reported that c-fos physically interacted with nuclear factor κB (NF-κB) p65 to inhibit transcription of TNF-α in response to pro-inflammatory cytokines such as lipopolysaccharide (LPS) in monocytic cells (Koga et al, Immunity, 2009). Therefore, we hypothesized that neutrophils with reduced c-fos would overproduce TNF-α in response to inflammatory stimuli in MDS. To test our hypothesis, siRNA for c-fos was introduced into HL60 cells that were differentiated toward a neutrophil-like phenotype by 1.25% DMSO. The treatment with siRNA decreased c-fos protein levels to 58.8 ± 19.6-fold of that in the control cells. When stimulated with 1 μM LPS for 3 hours, the increase rates of TNF-α mRNA were greater in c-fos siRNA-treated cells (41.2 ± 25.7-fold, p<0.05) than in the control cells (6.1 ± 2.3-fold). Chromatin immunoprecipitation assay demonstrated that LPS increased the binding of NF-κB p65 protein to the promoter region of TNF-α DNA by 2.7 ± 1.0-fold in the control cells. In c-fos siRNA-treated cells, the amounts of NF-κB p65 bound to the TNF-α DNA promoter without stimulation were 2.1 ± 0.3-fold greater than those in the unstimulated control cells, which was further increased to 5.6±0.3-fold by stimulation with LPS (p<0.05 compared to LPS-stimulated controls). These data suggested that neutrophils, as well as monocytic cells, transcribed greater amounts of TNF-α when c-fos was decreased. Neutrophils from patients with similar c-fos levels to those in the controls (Group A, n = 5), from the patients with reduced c-fos (Group B, n = 5), and from healthy controls (n = 8) were cultured in the presence of 1 μM LPS for 3 hours. TNF-α mRNA in control neutrophils was elevated 14.9 ± 3.2-fold. The increase in Group A was 10.1 ± 4.5-fold with no significant difference from the controls, while that in Group B was greater (31.5 ± 15.1-fold, p<0.05). Although neutrophils from Group A secreted similar amounts of TNF-α into the culture medium (143.5 ± 65.7 pg/mL) to the controls (150.6 ± 91.5 pg/mL), Group B produced significantly greater amounts of TNF-α (735.4 ± 65.7 pg/mL, p<0.05 vs. controls, p<0.05 vs. Group A). Thus, our data suggest that the reduction of c-fos resulting from aberrant expression of microRNAs contributes to overproduction of TNF-α under inflammatory stimuli in MDS. Disclosures No relevant conflicts of interest to declare.
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Vassilatou, D., Vassiliki Pappa, F. Kontsioti, S. Papageorgiou, C. Kontos, P. Tsirigotis, C. Economopoulou, E. Ioannidou, E. Papageorgiou, and Ioannis Dervenoulas. "Analysis of Let-7a and Mir-17-5p Micro-RNAs Expression In Patients with Adult De Novo Myelodysplastic Syndromes." Blood 116, no. 21 (November 19, 2010): 4965. http://dx.doi.org/10.1182/blood.v116.21.4965.4965.

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Abstract Abstract 4965 Introduction. MicroRNAs are small non-coding RNAs that act at the post-transcriptional level, regulating protein expression by repressing translation or destabilizing mRNA target. Since their discovery, microRNAs have been associated with almost every normal cell function, including proliferation, differentiation and apoptosis. Several studies suggest that they have an important role in normal hematopoiesis and hematological malignancies. Let-7a negatively regulates the expression of Ras proteins, which are overexpressed in patients with Myelodysplastic syndromes (MDS). In addition mir-17-5p contributes to the down-regulation of E2F1, which is overexpressed in MDS. Purpose. The purpose of the current study was to evaluate the expression of let-7a and mir-17-5p in CD34 cells from the bone marrow of patients with MDS. Material and methods. We evaluated 29 patients with MDS (25 men, 4 women) with median age 73 years. FAB classification was as follows: 9 RA, 15 RAEB, 2 RAEB-t and 3 AML. According to IPSS our study included 9 patients with low, 8 with Int-1, 7 with Int-2 and 5 with high risk disease. We isolated CD34+ cells from bone marrow of patients using magnetic beads. Extraction of microRNA and total RNA was performed and cDNA of let-7a and mir-17-5p was amplified using real time PCR, to study the relative expression of these microRNAS according to the expression of RNU48 (a snoRNA used as control). The control group included donors of CD34+ cells for stem cell transplantation. Results. The median miR17-5p expression level in patients was lower compared to controls [23vs 47.4]. The median let-7a expression levels were higher in MDS patients than in healthy donors [32.85 vs 8]. However these differences were not significant as shown by the Mann-Whitney U test. Moreover, ROC analysis demonstrated that neither miR17-5p nor let-7a expression had significant discriminatory value to efficiently distinguish MDS patients from non-MDS. In addition Spearman analysis did not reveal any correlations between these two microRNA expression levels and other continuous variables examined in the current study (age, hemoglobin concentration, numbers of neutrophils, platelets, and BM blasts). Finally, we found no associations between either miR17-5p or let-7a expression and clinicopathological parameters of MDS patients using chi-square (χ2) or Fisher's exact test where appropriate. Conclusion. The micro RNA let-7 was overexressed although not significantly in CD34 cells from MDS patients demonstrating that this is not a mechanism contributing to the increased expression RAS proteins in MDS. The micro RNA-mir17-5 is underexpressed in CD34 cells and needs further investigation for the establishment of a role in the overepxression of E2F in MDS. The lack of significant differences in the expression levels of both micro RNAs could be related to the admixture of normal and dysplastic CD34 cells in the bone marrow of MDS or to the small sample size. Disclosures: No relevant conflicts of interest to declare.
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Andre, E., E. Yaniz-Galende, C. Hamilton, G. J. Dusting, N. Hellen, CE Poulet, M. Diez Cunado, et al. "Poster session 1Cell growth, differentiation and stem cells - Heart72Understanding the metabolism of cardiac progenitor cells: a first step towards controlling their proliferation and differentiation?73Expression of pw1/peg3 identifies a new cardiac adult stem cell population involved in post-myocardial infarction remodeling74Long-term stimulation of iPS-derived cardiomyocytes using optogenetic techniques to promote phenotypic changes in E-C coupling75Benefits of electrical stimulation on differentiation and maturation of cardiomyocytes from human induced pluripotent stem cells76Constitutive beta-adrenoceptor-mediated cAMP production controls spontaneous automaticity of human induced pluripotent stem cell-derived cardiomyocytes77Formation and stability of T-tubules in cardiomyocytes78Identification of miRNAs promoting human cardiomyocyte proliferation by regulating Hippo pathway79A direct comparison of foetal to adult epicardial cell activation reveals distinct differences relevant for the post-injury response80Role of neuropilins in zebrafish heart regeneration81Highly efficient immunomagnetic purification of cardiomyocytes derived from human pluripotent stem cells82Cardiac progenitor cells posses a molecular circadian clock and display large 24-hour oscillations in proliferation and stress tolerance83Influence of sirolimus and everolimus on bone marrow-derived mesenchymal stem cell biology84Endoglin is important for epicardial behaviour following cardiac injuryCell death and apoptosis - Heart87Ultrastructural alterations reflecting Ca2+ handling and cell-to-cell coupling disorders precede occurrence of severe arrhythmias in intact animal heart88Urocortin-1 promotes cardioprotection through ERK1/2 and EPAC pathways: role in apoptosis and necrosis89Expression p38 MAPK and Cas-3 in myocardium LV of rats with experimental heart failure at melatonin and enalapril introductionTranscriptional control and RNA species - Heart92Accumulation of beta-amyloid 1-40 in HF patients: the role of lncRNA BACE1-AS93Role of miR-182 in zebrafish and mouse models of Holt-Oram syndrome94Mir-27 distinctly regulates muscle-enriched transcription factors and growth factors in cardiac and skeletal muscle cells95AF risk factors impair PITX2 expression leading to Wnt-microRNA-ion channel remodelingCytokines and cellular inflammation - Heart98Post-infarct survival depends on the interplay of monocytes, neutrophils and interferon gamma in a mouse model of myocardial Infarction99Inflammatory cd11b/c cells play a protective role in compensated cardiac hypertrophy by promoting an orai3-related pro-survival signal100Anti-inflammatory effects of endothelin receptor blockade in the atrial tissue of spontaneously hypertensive rats101Mesenchymal stromal cells reduce NLRP3 inflammasome activity in Coxsackievirus B3-induced myocarditis102Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis103The impact of regulatory T lymphocytes on long-term mortality in patients with chronic heart failure104Temporal dynamics of dendritic cells after ST-elevation myocardial infarction relate with improvement of myocardial functionGrowth factors and neurohormones - Heart107Preconditioning of hypertrophied heart: miR-1 and IGF-1 crosstalk108Modulation of catecholamine secretion from human adrenal chromaffin cells by manipulation of G protein-coupled receptor kinase-2 activity109Evaluation of cyclic adenosin-3,5- monophosphate and neurohormones in patients with chronic heart failureNitric oxide and reactive oxygen species - Heart112Hydrogen sulfide donor inhibits oxidative and nitrosative stress, cardiohemodynamics disturbances and restores cNOS coupling in old rats113Role and mechanisms of action of aldehydes produced by monoamine oxidase A in cardiomyocyte death and heart failure114Exercise training has contrasting effects in myocardial infarction and pressure-overload due to different endothelial nitric oxide synthase regulation115S-Nitroso Human Serum Albumin dose-dependently leads to vasodilation and alters reactive hyperaemia in coronary arteries of an isolated mouse heart model116Modulating endothelial nitric oxide synthase with folic acid attenuates doxorubicin-induced cardiomyopathy119Effects of long-term very high intensity exercise on aortic structure and function in an animal model120Electron paramagnetic resonance spectroscopy quantification of nitrosylated hemoglobin (HbNO) as an index of vascular nitric oxide bioavailability in vivo121Deletion of repressor activator protein 1 impairs acetylcholine-induced relaxation due to production of reactive oxygen speciesExtracellular matrix and fibrosis - Heart124MicroRNA-19b is associated with myocardial collagen cross-linking in patients with severe aortic stenosis. Potential usefulness as a circulating biomarker125A new ex vivo model to study cardiac fibrosis126Heterogeneity of fibrosis and fibroblast differentiation in the left ventricle after myocardial infarction127Effect of carbohydrate metabolism degree compensation to the level of galectin-3 changes in hypertensive patients with chronic heart failure and type 2 diabetes mellitus128Statin paradox in association with calcification of bicuspid aortic valve interstitial cells129Cardiac function remains impaired despite reversible cardiac fibrosis after healed experimental viral myocarditisIon channels, ion exchangers and cellular electrophysiology - Heart132Identifying a novel role for PMCA1 (Atp2b1) in heart rhythm instability133Mutations of the caveolin-3 gene as a predisposing factor for cardiac arrhythmias134The human sinoatrial node action potential: time for a computational model135iPSC-derived cardiomyocytes as a model to dissect ion current alterations of genetic atrial fibrillation136Postextrasystolic potentiation in healthy and diseased hearts: effects of the site of origin and coupling interval of the preceding extrasystole137Absence of Nav1.8-based (late) sodium current in rabbit cardiomyocytes and human iPSC-CMs138hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit cellular electrophysiological abnormalitiesMicrocirculation141Atherogenic indices, collagen type IV turnover and the development of microvascular complications- study in diabetics with arterial hypertension142Changes in the microvasculature and blood viscosity in women with rheumatoid arthritis, hypercholesterolemia and hypertensionAtherosclerosis145Shear stress regulates endothelial autophagy: consequences on endothelial senescence and atherogenesis146Obstructive sleep apnea causes aortic remodeling in a chronic murine model147Aortic perivascular adipose tissue displays an aged phenotype in early and late atherosclerosis in ApoE-/- mice148A systematic evaluation of the cellular innate immune response during the process of human atherosclerosis149Inhibition of Coagulation factor Xa increases plaque stability and attenuates the onset and progression of atherosclerotic plaque in apolipoprotein e-deficient mice150Regulatory CD4+ T cells from patients with atherosclerosis display pro-inflammatory skewing and enhanced suppression function151Hypoxia-inducible factor (HIF)-1alpha regulates macrophage energy metabolism by mediating miRNAs152Extracellular S100A4 is a key player of smooth muscle cell phenotypic transition: implications in atherosclerosis153Microparticles of healthy origins improve atherosclerosis-associated endothelial progenitor cell dysfunction via microRNA transfer154Arterial remodeling and metabolism impairment in early atherosclerosis155Role of pannexin1 in atherosclerotic plaque formationCalcium fluxes and excitation-contraction coupling158Amphiphysin II induces tubule formation in cardiac cells159Interleukin 1 beta regulation of connexin 43 in cardiac fibroblasts and the effects of adult cardiac myocyte:fibroblast co-culture on myocyte contraction160T-tubular electrical defects contribute to blunted beta-adrenergic response in heart failure161Beat-to-beat variability of intracellular Ca2+ dynamics of Purkinje cells in the infarct border zone of the mouse heart revealed by rapid-scanning confocal microscopy162The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: a study on transgenic mouse models with different mutations163Synthesis of cADPR and NAADP by intracellular CD38 in heart: role in inotropic and arrhythmogenic effects of beta-adrenoceptor signalingContractile apparatus166Towards an engineered heart tissue model of HCM using hiPSC expressing the ACTC E99K mutation167Diastolic mechanical load delays structural and functional deterioration of ultrathin adult heart slices in culture168Structural investigation of the cardiac troponin complex by molecular dynamics169Exercise training restores myocardial and oxidative skeletal muscle function from myocardial infarction heart failure ratsOxygen sensing, ischaemia and reperfusion172A novel antibody specific to full-length stromal derived factor-1 alpha reveals that remote conditioning induces its cleavage by endothelial dipeptidyl peptidase 4173Attenuation of myocardial and vascular arginase activity by vagal nerve stimulation via a mechanism involving alpha-7 nicotinic receptor during cardiac ischemia and reperfusion174Novel nanoparticle-mediated medicine for myocardial ischemia-reperfusion injury simultaneously targeting mitochondrial injury and myocardial inflammation175Acetylcholine plays a key role in myocardial ischaemic preconditioning via recruitment of intrinsic cardiac ganglia176The role of nitric oxide and VEGFR-2 signaling in post ischemic revascularization and muscle recovery in aged hypercholesterolemic mice177Efficacy of ischemic preconditioning to protect the human myocardium: the role of clinical conditions and treatmentsCardiomyopathies and fibrosis180Plakophilin-2 haploinsufficiency leads to impaired canonical Wnt signaling in ARVC patient181Improved technique for customized, easier, safer and more reliable transverse aortic arch banding and debanding in mice as a model of pressure overload hypertrophy182Late sodium current inhibitors for the treatment of inducible obstruction and diastolic dysfunction in hypertrophic cardiomyopathy: a study on human myocardium183Angiotensin II receptor antagonist fimasartan has protective role of left ventricular fibrosis and remodeling in the rat ischemic heart184Role of High-Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts activities and heart function after myocardial infarction185Atrial remodeling in hypertrophic cardiomyopathy: insights from mouse models carrying different mutations in cTnT186Electrophysiological abnormalities in ventricular cardiomyocytes from a Maine Coon cat with hypertrophic cardiomyopathy: effects of ranolazine187ZBTB17 is a novel cardiomyopathy candidate gene and regulates autophagy in the heart188Inhibition of SRSF4 in cardiomyocytes induces left ventricular hypertrophy189Molecular characterization of a novel cardiomyopathy related desmin frame shift mutation190Autonomic characterisation of electro-mechanical remodeling in an in-vitro leporine model of heart failure191Modulation of Ca2+-regulatory function by three novel mutations in TNNI3 associated with severe infant restrictive cardiomyopathyAging194The aging impact on cardiac mesenchymal like stromal cells (S+P+)195Reversal of premature aging markers after bariatric surgery196Sex-associated differences in vascular remodeling during aging: role of renin-angiotensin system197Role of the receptor for advanced glycation end-products (RAGE) in age dependent left ventricle dysfunctionsGenetics and epigenetics200hsa-miR-21-5p as a key factor in aortic remodeling during aneurysm formation201Co-inheritance of mutations associated with arrhythmogenic and hypertrophic cardiomyopathy in two Italian families202Lamin a/c hot spot codon 190: form various amino acid substitutions to clinical effects203Treatment with aspirin and atorvastatin attenuate cardiac injury induced by rat chest irradiation: Implication of myocardial miR-1, miR-21, connexin-43 and PKCGenomics, proteomics, metabolomics, lipidomics and glycomics206Differential phosphorylation of desmin at serines 27 and 31 drives the accumulation of preamyloid oligomers in heart failure207Potential role of kinase Akt2 in the reduced recovery of type 2 diabetic hearts subjected to ischemia / reperfusion injury208A proteomics comparison of extracellular matrix remodelling in porcine coronary arteries upon stent implantationMetabolism, diabetes mellitus and obesity211Targeting grk2 as therapeutic strategy for cancer associated to diabetes212Effects of salbutamol on large arterial stiffness in patients with metabolic syndrome213Circulating microRNA-1 and microRNA-133a: potential biomarkers of myocardial steatosis in type 2 diabetes mellitus214Anti-inflammatory nutrigenomic effects of hydroxytyrosol in human adipocytes - protective mechanisms of mediterranean diets in obesity-related inflammation215Alterations in the metal content of different cardiac regions within a rat model of diabetic cardiomyopathyTissue engineering218A novel conductive patch for application in cardiac tissue engineering219Establishment of a simplified and improved workflow from neonatal heart dissociation to cardiomyocyte purification and characterization220Effects of flexible substrate on cardiomyocytes cell culture221Mechanical stretching on cardiac adipose progenitors upregulates sarcomere-related genes." Cardiovascular Research 111, suppl 1 (July 1, 2016): S16—S42. http://dx.doi.org/10.1093/cvr/cvw135.

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Surmiak, Marcin, Katarzyna Wawrzycka-Adamczyk, Joanna Kosałka-Węgiel, Stanisław Polański, and Marek Sanak. "Profile of circulating extracellular vesicles microRNA correlates with the disease activity in granulomatosis with polyangiitis." Clinical and Experimental Immunology, March 3, 2022. http://dx.doi.org/10.1093/cei/uxac022.

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Abstract Granulomatosis with polyangiitis is a chronic systemic inflammation of small vessels characterized by circulating anti-proteinase 3 antibodies. MicroRNAs are short transcripts specifically inhibiting protein translation. Neutrophils can release extracellular vesicles (EVs). In this study, we characterized profile of microRNA trafficked by EVs in GPA. Fifty patients with GPA were enrolled in the study, 25 at acute phase and 25 in remission. EVs were isolated from the blood serum, characterized by their number, size distribution. Following unbiased screening for microRNA expression, differentially expressed candidates were measured by quantitative real-time PCR. Circulating DNA-myeloperoxidase complexes and apoptosis-related transcripts in peripheral blood neutrophils were quantified. We identified four differentially expressed microRNAs from EVs in granulomatosis with polyangiitis (GPA). MirRs-223-3p, 664a-3p, and 200b-3p were overexpressed and miR-769-5p suppressed in the disease. A distinction between GPA and healthy controls was the best for miR-223-3p, whereas miR-664a-3p discriminated between active vs. remission of GPA. Correct classification of the disease based on multivariate discriminant analysis was between 92% for acute phase and 85% for all study participants. Bioinformatics tools identified genes transcripts potentially targeted by the microRNAs belonging to pathways of focal adhesion, mTOR signaling and neutrophil extracellular traps formation. Two microRNAs positively correlating with the disease activity were involved in neutrophil extracellular traps formation and apoptosis inhibition. A comprehensive characteristics of microRNAs trafficked in bloodstream inside EVs correlates well with our understanding of the mechanisms of GPA and suggests the importance of EVs in progression of the disease.
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Dissertations / Theses on the topic "MicroRNA, Neutrophils, RNAsequencing, Apoptosis"

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Ghasemi, Somayehsadat. "Genome-wide analysis of human neutrophils mirnome identified miR-23a as a critical regulator of the apoptotic Fas antigen expression." Doctoral thesis, 2017. http://hdl.handle.net/11562/961048.

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Over the past decade, genome-wide studies have made it clear that the mammalian genome is pervasively transcribed and this led to the identification of non-protein coding RNA molecules. Only 2% of the mammalian genome accounts for protein-coding sequences, so that the majority is transcribed as noncoding RNA (ncRNA). ncRNAs appear to be highly conserved and are considered to be an important component for genetic regulation via epigenetic mechanisms. The regulatory ncRNAs can be classified into long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). miRNAs increasingly recognized to play a pivotal role in both physiological and pathological conditions, including mammalian development, cardiovascular, neurodegenerative and metabolic diseases, cancer and immune disorders. Despite the evidence for the importance of miRNAs in immune cell function and development, very limited information is available regarding how miRNAs regulate neutrophils development, lifespan and functions. Based on these premises, the purpose of this study was to provide a comprehensive analysis of microRNAs expression profile and to identify their role in primary human neutrophils under resting and stimulatory conditions. To achieve this goal we performed whole transcriptome analysis and characterized the pri-miRNome of resting and LPS-stimulated neutrophils. In parallel, the same analysis was performed also on autologous monocytes, in order to get insight into cell-specific miRNA profile. The results of this study showed that TLR4 engagement triggers the transcription of 37 pri-miRNAs. Additionally, comparison of LPS-induced pri-miRNA expression profile of neutrophils with that of autologous monocytes identified subsets of pri-miRNAs modulated by LPS in both cell type in a cell-specific manner. LPS induced the expression of twelve pri-miRNAs in neutrophils, among which we further validated the expression of the mature forms of the miR23a cluster members. The members of this cluster have been described to play important roles in various biological and pathological processes, but their role has never been previously identified in resting and/or activated neutrophils. Upon LPS stimulation neutrophils upregulate only the mature forms of miR-23a-5p and miR-27a-5p. In silico target prediction indicated Fas, a death receptor mediating cell apoptosis, among the miR-23a predicted target genes. Herein we provide several experimental proofs demonstrating that LPS reduces neutrophil Fas-induced apoptosis in a miR-23a-dependent manner. In fact, and consistent with a prolonged neutrophils’ half-life, in the presence of LPS a parallel upregulation of miR-23a and down-regulation of Fas membrane protein, but not Fas mRNA, expression was detected, suggesting involvement of a post-transcriptional regulation for Fas. Both Fas mRNA and miR-23a were detected in Ago immunoprecipitates only in LPS-stimulated neutrophils, thus indicating that LPS promotes miR-mediated post-transcriptional silencing of FAS. Finally, neutrophils overexpressing miR-23a reduced Fas membrane receptor. Taken together these data demonstrated that LPS stimulation affects neutrophil apoptosis via increasing miR-23a, which in return decreases the Fas expression on neutrophil surface. Collectively, we have described the expression profile of pri-miRNAs in resting and LPS-activated human neutrophils and their autologous monocytes, resulting in identification of cell type specific pri-miRNAs. The information from this whole transcriptome study led us to link the LPS to neutrophil apoptosis via miRNA modulation. Our data could be substantially used for further investigation on the role of miRNAs in neutrophils biology.
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