Articoli di riviste: "Matrix metalloproteinase 1 (MMP1)"

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Balasa, Rodica, Ciurba Bianca, Voidezan Septimiu, Simu Iunius, Hutanu Adina, Andone Sebastian, Romaniuc Andreea, Motataianu Anca, and Maier Smaranda. "The Matrix Metalloproteinases Panel in Multiple Sclerosis Patients Treated with Natalizumab: A Possible Answer to Natalizumab Non- Responders." CNS & Neurological Disorders - Drug Targets 17, no. 6 (August 28, 2018): 464–72. http://dx.doi.org/10.2174/1871527317666180703102536.

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Background: In the lymphocyte migration across the blood-brain barrier (BBB) in multiple sclerosis (MS), matrix metalloproteinases (MMPs) play an important role in the degradation of the basal membrane. Natalizumab (NAT), a monoclonal antibody, binds to the alpha-4 (α4) integrin leading to BBB impermeability. Approximately 30% of NAT-treated patients show clinical or MRI signs of BBB disruption. Objective: To determine whether NAT significantly influences the MMPs serum levels and to what extent these could be used as biomarkers in relapsing-remitting MS (RRMS) patients. Materials and Methods: This prospective study over a period of 8 months of NAT treatment, included 30 RRMS patients (mean age 38 ± 6 years; mean MS duration 12 ± 5 years), of which ten were initially naive to NAT and 15 were healthy controls. We determined the serum levels of the MMPs Panel (MMP1, MMP2, MMP3, MMP7, MMP8, MMP9, MMP10, MMP12, and MMP13) quantified by a multiplex method at the beginning and end of the study. Results: After 8 months of NAT treatment, a statistically significant decrease was found in MMP9, MMP2, MMP3, MMP8, and MMP10 levels. Relapses during the study were correlated with a variation of MMP12 and MMP13 serum levels. MMP9 had the most numerous correlations with the EDSS score, Rio score, and duration of NAT treatment. MMPs signature (the sum of all MMPs) and the MMP9/MMP2 ratio significantly decreased during the study. Conclusion: 1. The serum level of MMP9 significantly decreased by NAT treatment and correlates with MS activity; 2. After eight months of NAT treatment, the MMPs signature and the MMP9/MMP2 ratio decreased; 3. MMP9 might be used as a biomarker in MS patients treated with NAT.

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Skov, Vibe, Mads Thomassen, Lasse Kjær, Caroline Riley, Thomas Stauffer Larsen, Ole Weis Bjerrum, Torben A. Kruse, and Hans Carl Hasselbalch. "Extracellular Matrix-Related Genes Are Deregulated in Peripheral Blood from Patients with Myelofibrosis and Related Neoplasms." Blood 132, Supplement 1 (November 29, 2018): 5491. http://dx.doi.org/10.1182/blood-2018-99-117122.

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Abstract Introduction: The Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) which include essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF) are characterized by varying degrees of bone marrow fibrosis and endothelial proliferation. We and others have previously reported that these stromal alterations are reflected by increased serum levels of matrix derived metabolites, striated collagens type I/III and basement membrane components. The existence of a prefibrotic seromarker profile in MPNs is further evidenced by reports on increased serum levels of matrix metalloproteinase-3 (MMP-3) and decreased tissue inhibitor of metalloproteinase- I (TIMP-I). Using whole blood gene expression profiling, we aimed to provide a comprehensive gene signature of extracellular matrix-related proteins in MPNs with particular focus on genes associated with the regulation of major stromal proteins and MMPs. Methods: Gene expression profiling was performed on whole blood from 21 control subjects, 19 patients with ET, 41 patients with PV, and 9 patients with PMF. RNA was converted to biotin labeled amplified RNA (aRNA) using the MessageAmpTM III RNA amplification kit, and fragmented aRNA was hybridized to Affymetrix HG-U133 Plus 2.0 microarray chips recognizing 54,675 probe sets (38,500 genes). The R statistical software was applied to perform data preprocessing and statistical analysis of microarray data. Results: We identified 20,439, 25,307, and 17,417 probe sets that were differentially expressed between controls and patients with ET, PV, and PMF, respectively (FDR£0.05). These genes included 116 genes encoding extracellular matrix and adhesion molecules (ECM) important for cell-cell and cell-matrix interactions. These genes are represented on the Qiagen Human ECM panel, and in addition, all remaining collagen genes have been included. In patients with ET, COL1A1, COL1A2, COL3A1, COL4A2, COL4A5, LAMA2, LAMB1, MMP1, MMP7, MMP11, MMP12, MMP14, AND TIMP3 were among the 42 upregulated ECM genes (FDR<0.05). In patients with PV, 53 ECM genes were upregulated including COL1A1, COL1A2, COL3A1, COL4A2, LAMA2, LAMB1, MMP1, MMP7, MMP8, MMP9, MMP11, MMP12, MMP14, and TIMP3 (FDR<0.05). In PMF, COL1A2, COL3A1, COL4A2, COL4A5, LAMA2, MMP1, MMP8, MMP9, MMP14, and TIMP3 were among the 26 upregulated genes (FDR<0.05) (Table 1). 17, 14, and 13 ECM genes were significantly downregulated in ET, PV, and PMF, respectively (FDR<0.05) (data not shown). ITGA7, ITGB3, and MMP1 were significantly upregulated from ET over PV to PMF, whereas ITGAL, SPG7, and TGFBI were significantly downregulated from ET over PV to PMF. ADAMTS8, ADAMTS13, COL10A1, COL14A1, COL1A2, COL29A1, COL3A1, COL4A2, COL6A1, ITGA7, ITGB3, ITGB5, LAMA2, MMP1, MMP14, NCAM1, THBS2, and TIMP3 were significantly upregulated in both ET, PV, and PMF (FDR<0.05). COL4A3BP, COL6A2, ITGA4, ITGA5, ITGAL, ITGB1, PECAM1, SPG7, and TGFBI were significantly downregulated in both ET, PV, and PMF (FDR<0.05). In table 2a-b are shown the 10 most significantly up- and downregulated genes. Discussion and conclusions: Bone marrow fibrosis and endothelial proliferation in MPNs are elicited due to the release of fibrogenic and angiogenic growth factors primarily from hyperproliferating megakaryocytes. The connective tissue components of the bone marrow in MPNs include type III collagen, which is deposited in the early disease stages (ET/PV) as "reticulin fibrosis" being accompanied and substituted by mature Van Giesson positive collagen (type I collagen) in the advanced myelofibrosis stage. Increased endothelial cell proliferation is followed by the development of continuous sheets of basement membrane material beneath endothelial cells as assessed by increased deposition of type IV collagen and laminin. Using whole blood gene expression profiling, we provide evidence that abnormal extracellular matrix metabolism is reflected in the gene signature of peripheral blood cells from patients with MPNs. Further studies are needed to determine whether these changes represent local bone marrow fibrogenesis and/or systemic disease manifestations. Disclosures Hasselbalch: Novartis: Research Funding.

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Mogulevtseva, J. A., A. V. Mezentsev, and S. A. Bruskin. "RNAI-MEDIATED SILENCING OF MATRIX METALLOPROTEINASE 1 IN EPIDERMAL KERATINOCYTES INFLUENCES THE BIOLOGICAL EFFECTS OF INTERLEUKIN 17A." Vavilov Journal of Genetics and Breeding 22, no. 4 (July 3, 2018): 425–32. http://dx.doi.org/10.18699/vj18.378.

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Matrix metalloproteinases (MMPs) are important for the pathogenesis of psoriasis and other autoimmune disorders. In the extracellular matrix, accumulation of proinflammatory cytokines, such as interleukin 17A (IL-17A), leads to induction of several MMPs, including MMP1. MMPs change the composition and other properties of the extracellular matrix. These changes facilitate tissue remodeling and promote the development of psoriatic plaques. The aim of this study was to explore how MMP1 silencing might influence the biological effects of IL-17A on migration and proliferation of human epidermal keratinocytes and the expression of genes involved in their division and differentiation. The experiments were performed with MMP1-deficient and control epidermal keratinocytes, HaCaT-MMP1 and HaCaT-KTR, respectively. Cell proliferation and migration were assessed by comparative analysis of the growth curves and scratch assay, respectively. To quantify cell migration, representative areas of cell cultures were photographed at the indicated time points and compared to each other. Changes in gene expression were analyzed by real-time PCR. The obtained results demonstrated that MMP1 silencing in the cells treated with IL-17A resulted in downregulation of MMP9 and -12, FOSL1, CCNA2, IVL, KRT14 and -17 as well as upregulation of MMP2, CCND1 and LOR. Moreover, MMP1 silencing led to a decrease in cell proliferation and an impairment of cell migration. Thus, MMP1-deficiency in epidermal keratinocytes can be beneficial for psoriasis patients that experience an accumulation of IL-17 in lesional skin. Knocking MMP1 down could influence migration and proliferation of epidermal keratinocytes in vivo, as well as help to control the expression of MMP1, -2, -9 и -12, CCNA2, CCND1, KRT14 and -17 that are crucial for the pathogenesis of psoriasis.

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Chen, Chao, Congcong Li, Weichun Liu, Feng Guo, Xi Kou, Si Sun, Taiyang Ye, Shanji Li, and Aimin Zhao. "Estrogen-induced FOS-like 1 regulates matrix metalloproteinase expression and the motility of human endometrial and decidual stromal cells." Journal of Biological Chemistry 295, no. 8 (January 14, 2020): 2248–58. http://dx.doi.org/10.1074/jbc.ra119.010701.

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The regulation mechanisms involved in matrix metalloproteinase (MMP) expression and the motility of human endometrial and decidual stromal cells (ESCs and DSCs, respectively) during decidualization remain unclear. DSCs show significant increased cell motility and expression of FOS-like 1 (FOSL1) and MMP1, MMP2, and MMP9 compared with ESCs, whereas lack of decidualization inducers leads to a rapid decrease in FOSL1 and MMP1 and MMP9 expression in DSCs in vitro. Therefore, we hypothesized that a link exists between decidualization inducers and FOSL1 in up-regulation of motility during decidualization. Based on the response of ESCs/DSCs to different decidualization systems in vitro, we found that progesterone (P4) alone had no significant effect and that 17β-estradiol (E2) significantly increased cell motility and FOSL1 and MMP1 and MMP9 expression at the mRNA and protein levels, whereas 8-bromo-cAMP significantly decreased cell motility and FOSL1 and MMP9 expression in the presence of P4. In addition, we showed that E2 triggered phosphorylation of estrogen receptor 1 (ESR1), which could directly bind to the promoter of FOSL1 in ESCs/DSCs. Additionally, we also revealed silencing of ESR1 expression by siRNA abrogated E2-induced FOSL1 expression at the transcript and protein levels. Moreover, silencing of FOSL1 expression by siRNA was able to block E2-induced MMP1 and MMP9 expression and cell motility in ESCs/DSCs. Taken together, our data suggest that, in addition to its enhancement of secretory function, the change in MMP expression and cell motility is another component of the decidualization of ESCs/DSCs, including estrogen-dependent MMP1 and MMP9 expression mediated by E2–ESR1–FOSL1 signaling.

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Zhang, Jianmei, Mi-Yeon Kim, and Jae Youl Cho. "Euodia pasteuriana Methanol Extract Exerts Anti-Inflammatory Effects by Targeting TAK1 in the AP-1 Signaling Pathway." Molecules 25, no. 23 (December 7, 2020): 5760. http://dx.doi.org/10.3390/molecules25235760.

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Euodia pasteuriana A. Chev. ex Guillaumin, also known as Melicope accedens (Blume) T.G. Hartley, is a herbal medicinal plant native to Vietnam. Although Euodia pasteuriana is used as a traditional medicine to treat a variety of inflammatory diseases, the pharmacological mechanisms related to this plant are unclear. This study aimed to investigate the anti-inflammatory effects of a methanol extract of Euodia pasteuriana leaves (Ep-ME) on the production of inflammatory mediators, the mRNA expression of proinflammatory genes, and inflammatory signaling activities in macrophage cell lines. The results showed that Ep-ME strongly suppressed the release of nitric oxide (NO) in RAW264.7 cells induced with lipopolysaccharide (LPS), pam3CysSerLys4 (Pam3CSK), and polyinosinic-polycytidylic acid (poly I:C) without cytotoxicity. A reverse transcription-polymerase chain reaction further confirmed that Ep-ME suppressed the expression of interleukin 6 (IL-6), matrix metalloproteinase-1 (MMP1), matrix metalloproteinase-2 (MMP2), matrix metalloproteinase-3 (MMP3), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-9 (MMP9) at the transcriptional level and reduced the luciferase activities of activator protein 1 (AP-1) reporter promoters. In addition, immunoblotting analyses of the whole lysate and nuclear fraction, as well as overexpression assays demonstrated that Ep-ME decreased the translocation of c-Jun and suppressed the activation of transforming growth factor beta-activated kinase 1 (TAK1) in the AP-1 signaling pathways. These results imply that Ep-ME could be developed as an anti-inflammatory agent that targets TAK1 in the AP-1 signaling pathway.

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Zaidi, Sana Jafar, Nabeela Riaz, Asifa Iqbal, and Ayyaz Ali Khan. "Salivary Matrix Metalloproteinase (MMP)-1 as Non-Invasive Tool for The Diagnosis of Oral Squamous Cell Carcinoma (OSCC)." Journal of the Pakistan Dental Association 30, no. 1 (February 14, 2021): 18–23. http://dx.doi.org/10.25301/jpda.301.18.

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OBJECTIVE: To determine the diagnostic accuracy of salivary MMP1 as non-invasive diagnostic biomarker of OSCC through conventional sandwich ELISA technique. Analytical cross-sectional study. METHODOLOGY: Individuals with clinical suspicion for OSCC (IWCS-OSCC) were included in the study after fulfilling selection criteria. Saliva samples were collected from IWCS-OSCC. To confirm OSCC, the patients were referred for biopsy. After definitive diagnosis on biopsy, patients were labeled OSCC positive or OSCC negative. The colorimetric sandwich-ELISA test was performed on saliva samples to measure the level of MMP1. Data was entered in "Statistical Package for the Social Sciences (SPSS) -16" and levels of MMP1 were correlated with the biopsy status of patient (OSCC positive or OSCC negative). RESULTS: Our sample included twice as many males as females (2.1:1) and a wide age range of 22-77years with median age of 50yrs. Of all the IWCS-OSCC 85% were OSCC +ve and 15% were OSCC-ve. Diagnostic accuracy was measured as; Area under curve (AUC) = 0.623, Sensitivity (Sn) = 50%, Specificity (Sp)= 83.3%, Positive predictive value (PPV)= 94.4%, Negative predictive value (NPV)= 22.7% CONCLUSION: MMP1 as detected by conventional sandwich-ELISA technique is not proven as an accurate diagnostic biomarker of OSCC. KEY WORDS: OSCC; MMP1; IWCS-OSCC; Sandwich-ELISA HOW TO CITE: Zaidi SJ, Riaz N, Iqbal A, Khan AA. Salivary matrix metalloproteinase (MMP)-1 as non-invasive tool for the diagnosis of oral squamous cell carcinoma (OSCC). J Pak Dent Assoc 2021;30(1):18-23.

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Korytina, G. F., L. Z. Akhmadishina, D. G. Yanbaeva, Sh Z. Zagidullin, and T. V. Viktorova. "Association of polymorphic variants of matrix metalloproteinase and antiprotease genes with development and severity of chronic obstructive pulmonary disease." PULMONOLOGIYA, no. 1 (February 28, 2008): 33–38. http://dx.doi.org/10.18093/0869-0189-2008-0-1-33-38.

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To evaluate a role of polymorphic variants of metalloproteinase and protease genes for hereditary susceptibility to COPD and its severity, we analyzed polymorphic loci of MMP1, MMP9, MMP12, PI, and AACT genes in COPD patients (n = 318) and healthy persons (n = 319) living at the Bashkortostan Republic. Results showed that frequency of genotypes and alleles of G(-1607)GG gene MMP1, С(-1562)T gene MMP9, A(-82)G gene MMP12, and Ala 15 Thr gene ААСТ did not differ in COPD patients and healthy subjects. The Zand S-mutations of the PI gene were also similar in both the groups. The heterozygous GA genotype of G1237A locus in the 3'-non-translated region of PI gene was associated with COPD occurrence (OR = 2.09; 95 % CI: 1.15–3.81). To determine polymorphic variants associated with severity of clinical course and age of the disease manifestation, a comparative analysis of rates of genotypes and alleles was performed in patients with different COPD stages and of different age. The stage IV COPD patients significantly more often carried rare T allele in С(-1562)T locus of the MMP9 gene (15.89 % vs 8.38 %; χ2 = 7.804; df = 1; p = 0.005; OR = 2.06; 95 % CI: 1.22–3.49). Individuals with rare TT genotype of MMP9 gene were found only among the stage IV COPD patients (3.97 % vs 0 %; χ2 = 4.78; p = 0.029; pcor = 0.058). Moreover, analysis of this locus in patients with early manifestation of COPD (younger the 55 yrs) revealed significantly more frequent rate of T allele in patients with stage IV COPD compared to patients of the same age but less severe COPD (χ2 = 5.26; df = 1; p = 0.022).

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Morais Junior, Gilberto Santos, Nathalia Oliveira Rodrigues, Adriane Dallanora Henriques, Audrey Cecília Tonet-Furioso, Ciro José Brito, Lucy Oliveira Gomes, Clayton Franco Moraes, and Otávio Toledo Nóbrega. "Matrix Metalloproteinase-1 Gene Polymorphism Associated with Ultrasound-Assessed Carotid Thickness among Older Adults." Journal of Aging Research 2018 (June 21, 2018): 1–6. http://dx.doi.org/10.1155/2018/1475890.

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Background and Aim. Due to the high incidence of vascular diseases, it is necessary to identify new circulating or structural markers for predicting risk for chronic diseases. Some studies suggest that MMP1 gene polymorphisms are associated with the enzyme expression levels in situ (e.g., in atherosclerotic plaques). Objectives. Thus, the study of this polymorphism may help understanding the pathophysiology of coronary disease. Methods. We performed cross-sectional clinical and laboratory evaluations (including measurement of intima-media thickness of carotid arteries) and genotyping of the MMP1 SNP rs495366 (A/G) in 366 elderly people. Results. No significant differences between genotypes were noted for biochemical, metabolic, inflammatory, or clinical variables except for a significant difference in intima-media thickness for the left carotid artery and a trend toward significance for the right counterpart. Conclusion. Carriers of the allele associated with lower MMP1 expression (allele A) presented greater carotid thickness. We suggest that the phenomenon can be explained by impaired remodeling of the arterial wall (poor degradation of collagen fibers in this scenario), yielding carotid wall thickening and a greater intrinsic risk for cerebrovascular events.

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Said, Anan H., Shien Hu, Ameer Abutaleb, Tonya Watkins, Kunrong Cheng, Ahmed Chahdi, Panjamurthy Kuppusamy, Neeraj Saxena, Guofeng Xie, and Jean-Pierre Raufman. "Interacting post-muscarinic receptor signaling pathways potentiate matrix metalloproteinase-1 expression and invasion of human colon cancer cells." Biochemical Journal 474, no. 5 (February 20, 2017): 647–65. http://dx.doi.org/10.1042/bcj20160704.

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M3 muscarinic receptor (M3R) expression is increased in colon cancer; M3R activation stimulates colon cancer cell invasion via cross-talk with epidermal growth factor receptors (EGFR), post-EGFR activation of mitogen-activated protein kinase (MAPK) extracellular signal-related kinase 1/2 (ERK1/2), and induction of matrix metalloproteinase-1 (MMP1) expression. MMP1 expression is strongly associated with tumor metastasis and adverse outcomes. Here, we asked whether other MAPKs regulate M3R agonist-induced MMP1 expression. In addition to activating ERK1/2, we found that treating colon cancer cells with acetylcholine (ACh) stimulated robust time- and dose-dependent phosphorylation of p38 MAPK. Unlike ERK1/2 activation, ACh-induced p38 phosphorylation was EGFR-independent and blocked by inhibiting protein kinase C-α (PKC-α). Inhibiting activation of PKC-α, EGFR, ERK1/2, or p38-α/β alone attenuated, but did not abolish ACh-induced MMP1 expression, a finding that predicted potentiating interactions between these pathways. Indeed, ACh-induced MMP1 expression was abolished by incubating cells with either an EGFR or MEK/ERK1/2 inhibitor combined with a p38-α/β inhibitor. Activating PKC-α and EGFR directly with the combination of phorbol 12-myristate 13-acetate (PMA) and EGF potentiated MMP1 gene and protein expression, and cell invasion. PMA- and ACh-induced MMP1 expression were strongly diminished by inhibiting Src and abolished by concurrently inhibiting both p38-α/β and Src, indicating that Src mediates the cross-talk between PKC-α and EGFR signaling. Using siRNA knockdown, we identified p38-α as the relevant p38 isoform. Collectively, these studies uncover novel functional interactions between post-muscarinic receptor signaling pathways that augment MMP1 expression and drive colon cancer cell invasion; targeting these potentiating interactions has therapeutic potential.

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Sauter, Wiebke, Albert Rosenberger, Lars Beckmann, Silke Kropp, Kirstin Mittelstrass, Maria Timofeeva, Gabi Wölke, et al. "Matrix Metalloproteinase 1 (MMP1) Is Associated with Early-Onset Lung Cancer." Cancer Epidemiology Biomarkers & Prevention 17, no. 5 (May 2008): 1127–35. http://dx.doi.org/10.1158/1055-9965.epi-07-2840.

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Moskalenko, M. I., S. N. Milanova, I. V. Ponomarenko, A. V. Polonikov, and M. I. Churnosov. "Study of associations of polymorphism of matrix metalloproteinases genes with the development of arterial hypertension in men." Kardiologiia 59, no. 7S (August 23, 2019): 31–39. http://dx.doi.org/10.18087/cardio.2598.

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The aim of research. To study the association of polymorphic loci of matrix metalloproteinases with the development of essential hypertension (EH) in men of the Central Chernozem Region of Russia. Materials and methods. A study of 564 men with EH and 257 control men was performed. Analysis of the polymorphic loci of metalloproteinases rs11568818 MMР7, rs1320632 MMР8, rs11225395 MMР8, rs1799750 MMР1, rs3025058 MMР3 was performed using real-time PCR. The study of associations of SNPs and their haplotypes with the development of arterial hypertension was carried out using logistic regression analysis in the PLINK software (v. 2.050). The regulatory potential of polymorphic loci was analyzed in the HaploReg software (v. 4.1) (http://archive.broadinstitute.org). The effect of SNP on gene expression was studied using the data of the Genotype-Tissue Expression project (http://www.gtexportal.org/). Results. Haplotype including rs11568818 MMP7, rs1320632 MMP8, rs11225395 MMP8 and rs1799750 MMP1 associated with a high risk of disease in men (OR=2,58, pperm=0,04). These polymorphisms located in region of promoter and enhancer histone marks and in the region of hypersensitivity to DNAse-1. They located in sites of proteins bound (TBP, CJUN, CFOS and GATA2) and they associated with the level of gene expression ММР7, ММР27 and RP11-817J15.3 (in peripheral blood, skeletal muscles, nervous tissue and other). Сonclusion. Haplotype G-A-C-1G for polymorphisms rs11568818 MMP7, rs1320632 MMP8, rs11225395 MMP8, rs1799750 MMP1 are associated with the development of essential hypertension in men in the Central Chernozem Region of Russia.

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Leite, Sergio Roberto de Andrade. "Inhibitors of human collagenase, MMP1." Eclética Química 34, no. 4 (December 2009): 87–102. http://dx.doi.org/10.1590/s0100-46702009000400008.

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Different common drugs (Meloxicam, Tenoxicam and Piroxicam, and sodium alendronate) were tested both experimental and theoretically as inhibitors of interstitial human collagenase, also known as matrix metalloproteinase 1 (MMP-1). The in vitro collagenase activity, alone and in the presence of inhibitors, was quantified by the reaction with a fluorescent synthetic substrate and measuring the change of emission. Collagenase-inhibitor interaction was studied theoretically by computational calculations. Three among the four tested substances showed moderate inhibiting activity against the human collagenase.

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Leite, Sergio Roberto De Andrade. "Inhibitors of human collagenase, MMP1." Eclética Química Journal 39, no. 4 (January 30, 2018): 87. http://dx.doi.org/10.26850/1678-4618eqj.v39.4.2009.p87-102.

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Different common drugs (Meloxicam, Tenoxicam and Piroxicam, and sodium alendronate) were tested both experimental and theoretically as inhibitors of interstitial human collagenase, also known as matrix metalloproteinase 1 (MMP-1). The in vitro collagenase activity, alone and in the presence of inhibitors, was quantified by the reaction with a fluorescent synthetic substrate and measuring the change of emission. Collagenase-inhibitor interaction was studied theoretically by computational calculations. Three among the four tested substances showed moderate inhibiting activity against the human collagenase.

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Calascibetta, A., V. Gebbia, D. Cabibi, A. Martorana, F. Aragona, L. Rausa, and R. Sanguedolce. "Matrix metalloproteinase-1 is differentially expressed in signet ring cell, and intestinal colorectal carcinomas histotypes." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 14564. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14564.

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14564 Background: Signet ring cell colorectal carcinoma ( SRCC) pure is an infrequent and highly malignant variant of colorectal cancer, while this histological component is present in 30% of all colorectal carcinomas. In our previous studies we compared the E- Cadherin, β- Catenin, Fibronectin, Ki 67 and Thymidylate Synthase (TS) expression of SRCC, the intestinal type of colorectal carcinoma (ICRC) to try to explain the pathogenesis, the aggressiveness and the low 5 Fluorouracil (5FU) responsiveness of these tumours. We found that all SRCCs had very low levels of all markers and were in the post- mitotic phase of the cell cycle. To understand their high metastatic capability we assessed the SRCC expression of Matrix Metallo Proteinase-1 (MMP1), a proteolytic enzyme, suspected to play an important role in the progression of various cancer and compared it to the ICRC one. Methods: We tested MMP1 expression immunohistochemically on formalin-fixed, paraffin-embedded samples of 32 SRCC and 70 ICRC. Differences in the distribution of the study variables, and associations between variables were assessed by means of the ?2 test. Results: SRCC showed a high expression of MMP1 over all in the invasion front of the tumour and in the neoplastic embolus rather then the ICRC (p<0.001). Conclusions: As MMPs seem to play important role in tumour invasion and metastasis, recently they have gained attention as targets for new anticancer therapy strategies. MMPs inhibitors have been shown to prevent tumour spread both in vitro and in vivo and to inhibit tumour angiogenesis and some of them are being developed for clinical use. In these study we demonstrated that SRCCs showed a different MMP1 expression pattern from the ICRC one, for this reason an anti-MMP therapy should be advisable in these patients, because of their bad prognosis. No significant financial relationships to disclose.

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Fanjul-Fernández, Miriam, Alicia R. Folgueras, Antonio Fueyo, Milagros Balbín, María F. Suárez, M. Soledad Fernández-García, Steven D. Shapiro, José M. P. Freije, and Carlos López-Otín. "Matrix Metalloproteinase Mmp-1a Is Dispensable for Normal Growth and Fertility in Mice and Promotes Lung Cancer Progression by Modulating Inflammatory Responses." Journal of Biological Chemistry 288, no. 20 (April 2, 2013): 14647–56. http://dx.doi.org/10.1074/jbc.m112.439893.

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Human MMP-1 is a matrix metalloproteinase repeatedly associated with many pathological conditions, including cancer. Thus, MMP1 overexpression is a poor prognosis marker in a variety of advanced cancers, including colorectal, breast, and lung carcinomas. Moreover, MMP-1 plays a key role in the metastatic behavior of melanoma, breast, and prostate cancer cells. However, functional and mechanistic studies on the relevance of MMP-1 in cancer have been hampered by the absence of an in vivo model. In this work, we have generated mice deficient in Mmp1a, the murine ortholog of human MMP1. Mmp1a−/− mice are viable and fertile and do not exhibit obvious abnormalities, which has facilitated studies of cancer susceptibility. These studies have shown a decreased susceptibility to develop lung carcinomas induced by chemical carcinogens in Mmp1a−/− mice. Histopathological analysis indicated that tumors generated in Mmp1a−/− mice are smaller than those of wild-type mice, consistently with the idea that the absence of Mmp-1a hampers tumor progression. Proteomic analysis revealed decreased levels of chitinase-3-like 3 and accumulation of the receptor for advanced glycation end-products and its ligand S100A8 in lung samples from Mmp1a−/− mice compared with those from wild-type. These findings suggest that Mmp-1a could play a role in tumor progression by modulating the polarization of a Th1/Th2 inflammatory response to chemical carcinogens. On the basis of these results, we propose that Mmp1a knock-out mice provide an excellent in vivo model for the functional analysis of human MMP-1 in both physiological and pathological conditions.

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Rosales, Alberto Sierra, Eduardo Alberto Villaseñor Rodríguez, Christian Lorena López González, Edy David Rubio Arellano, Susan Andrea Gutiérrez Rubio, and Teresa Arcelia García Cobián. "Association Between -1607 1G/2G Polymorphism of MMP1 and Temporomandibular Joint Anterior Disc Displacement with Reduction." Brazilian Dental Journal 31, no. 2 (April 2020): 152–56. http://dx.doi.org/10.1590/0103-6440202003037.

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Abstract Anterior disc displacement with reduction (DDWR) is considered one of the most common disorders within the temporomandibular joint (TMJ), with a prevalence of 41% in adults. Matrix metalloproteinases play an important role in the degradation of the TMJ and the matrix metalloproteinase 1 (MMP1) 1607 1G/2G polymorphism increases the local expression of MMP1 thus leading to accelerated degradation of the extracellular matrix. The objective of this study was to evaluate the association between the 1607 1G/2G polymorphism of MMP1 gene and DDWR in a group of Mexican individuals from western Mexico. A total of 67 unrelated individuals, between the ages of 18 and 36 years, of both genders, were included in this study. Study participants with DDWR were required to meet the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD), while a second control group of 90 individuals without DDWR were also included. Both groups were required to have paternal and maternal ancestry (grandparents) of the same geographic and ethnic region. Genotypes were determined using the nested PCR technique. The 1G/2G polymorphism was found in 68.7%, followed by 2G/2G in 25.4% and 1G/1G in 6.0% of the cases group. While the prevalence in the control group was 55.5% for the 1G/2G polymorphism, 26.6% for 1G/1G and 17.7% for 2G/2G. An association was found between the 2G allele of the 1607 1G/2G polymorphism of MMP1 gene and the presence of DDWR in the patients of western Mexico.

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Srivastava, Priyanka, Ruchika Gangwar, Rakesh Kapoor, and Rama D. Mittal. "Bladder Cancer Risk Associated with Genotypic Polymorphism of the Matrix Metalloproteinase-1 and 7 in North Indian Population." Disease Markers 29, no. 1 (2010): 37–46. http://dx.doi.org/10.1155/2010/149651.

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Matrix metalloproteinases (MMPs) contribute to tumor invasion and microenvironment, hence are associated with bladder cancer risk. We therefore, tested whether polymorphisms in MMP genes modify the risk of bladder cancer (BC) and whether smoke exposure modifies this risk.Genotyping was performed in 200 BC patients and 200 controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).MMP1-1607 2G/2G andMMP7-181 GG genotype were associated with increased risk of BC (p<0.001; OR, 3.04; 95% CI1.71–5.39 and p, 0.005; OR, 2.38; 95% CI1.30–4.34) respectively. Smokers in BC patients showed significant increased risk for the same SNPs (p, 0.006; OR, 3.20; 95% CI1.40–7.31 and p, 0.009; OR, 2.85; 95% CI1.30–6.23 respectively). Haplotype analysis too revealed significant association with G/2G ofMMP1-519-1607 (p< 0.001; OR, 2.62; 95% CI1.68–4.09). The 2G allele carrier (1G/2G + 2G/2G) ofMMP1-1607 showed a protective effect and high recurrence free survival in Bacillus Calmette-Guerin (BCG) treated non muscle invasive BC (NMIBC) patients (log rank p, 0.030). Our datasuggested that MMP11607 2G and MMP7181 G allele were associated with high risk of BC, which was quite evident amongst smokers too. BCG treated NMIBC patients reflected protective effect for 2G allele carrier (1G/2G+2G/2G) ofMMP1-1607. This study provided new support for the association of MMP1-1607 and MMP7-181 in bladder cancer development, the tumorigenic effect of which was observed to be more enhanced in case of tobacco exposure.

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Wathes, D. Claire, Zhangrui Cheng, Mark A. Fenwick, Richard Fitzpatrick, and Joe Patton. "Influence of energy balance on the somatotrophic axis and matrix metalloproteinase expression in the endometrium of the postpartum dairy cow." REPRODUCTION 141, no. 2 (February 2011): 269–81. http://dx.doi.org/10.1530/rep-10-0177.

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Postpartum dairy cows enter a period of negative energy balance (NEB) associated with low circulating IGF1, during which the uterus must undergo extensive repair following calving. This study investigated the effects of NEB on expression of IGF family members and related genes in the involuting uterus. Cows were allocated to two treatments using differential feeding and milking regimes to produce mild NEB or severe NEB (SNEB). Uterine endometrial samples collected 2 weeks post partum were analysed by quantitative PCR. The expression of IGF-binding protein 4 (IGFBP4) mRNA increased in the endometrium of SNEB cows, with trends towards increased IGFBP1 and reduced IGFBP6 expression. There were no significant differences between treatments in mRNA expression of IGF1, IGF2 or of any hormone receptor studied, but significant correlations across all cows in the expression levels of groups of receptors suggested common regulatory mechanisms: type 1 IGF receptor (IGF1R), IGF2R and insulin receptor (INSR); GHR with ESR1; and ESR2 with NR3C1. The expression of IGF1R and INSR also positively correlated with the circulating urea concentration. Matrix metalloproteinases (MMPs) are important in tissue remodelling and can affect IGF signalling via interaction with IGFBPs. The expression levels of MMP1, MMP3, MMP9 and MMP13 mRNAs all showed major upregulation in the endometrium of cows in SNEB and all except MMP9 were highly correlated with expression of IGFBP4. Alpha(2)-HS-glycoprotein (AHSG) and PDK4, two genes implicated in insulin resistance, were also highly expressed in SNEB. These results suggest that cows in SNEB experience alterations to the IGF and insulin signalling pathways in the postpartum endometrium. This may affect the rate of tissue repair with a possible negative impact on subsequent fertility.

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Rohil, Vishwajeet, V. K. Vijayan, Raj Kumar, Rini Joshi, P. Pavani, Shweta Paul, Anju Sharma, and Mujeeb Ur Rahman. "A study on the correlation of matrix metalloproteinase MMP1 in COPD and smoking in the North Indian population." Asian Journal of Medical Sciences 8, no. 1 (January 3, 2017): 5–14. http://dx.doi.org/10.3126/ajms.v8i1.16020.

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Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by airway obstruction and destruction of lung tissue, the disease for which at present there is no cure, although the treatment can slow worsening. Nearly 90% of COPD is caused by long term cigarette smoking; however, only 25% of chronic tobacco smokers develop COPD, the exact cause of this predisposition of some smokers to acquire COPD is still poorly understood at the molecular level. Lot of studies are available showing the correlation of MMP1 and asthma but not much work has been done on its correlation with COPD especially in North India. The outcome of our study was also expected to discover MMP1 as a new target for treating COPD and its progression in smokers.Aim and Objectives: The association of COPD and smoking with MMP1 gene product and its SNP in the North Indian population was intended to be studied.Material and Methods: The proposed study was a case control study. In this study adults aged 30 years and above fulfilling the inclusion criteria (Please see Annexure I) were considered and a total of 180 subjects were taken after determining the sample size. Pulmonary function test (PFT) was performed by Spirometry. Three main groups each consisting of 60 subjects were formed on the basis of smoking history and Spirometry: Ist group: Smokers without co-morbidity with normal PFT, IInd group: Smokers with Spirometry proved COPD and without any other co-morbidity, IIIrd group: Healthy Non-smoker controls. Quantification of metalloproteinase MMP1 in all the groups were performed in the serum with ELISA kits and Single Nucleotide Polymorphism (SNP 1G-1607 2G, ID rs1799750) studies in the gene encoding MMP1 linked to COPD susceptibility in smokers was performed by DNA Sequencing Analysis. The correlation between the SNPs, gene product, smoking and COPD was studied. Results: MMP1 concentration was seen increased in serum of COPD and smokers when compared to healthy controls. And there is high negative correlation between *FEV1/FVC % (post-bronchodilator) and MMP1 in COPD compared to Smokers and Healthy Controls. However, from the results of present analysis, we could show negative correlation between MMP1 and *FEV1/FVC % in all the 3 groups but the correlation proves to be much more negative in Group II i.e. Smokers with COPD. Statistically Significant Positive Correlation of Pack Years with MMP1 conc., and Statistically Significant Negative Correlation between Pack Years and *FEV1/FVC % was seen.Conclusion:In conclusion, our present analyses did show significant association between MMP1 and COPD risk in North Indian population. MMP1 levels of COPD patients were significantly increased in smokers and may contribute to or be a marker of the pathophysiology of COPD. Asian Journal of Medical Sciences Vol.8(1) 2017 5-14

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Fu, Sai C., Barbara P. Chan, Wen Wang, Hon M. Pau, Kai M. Chan, and Christer G. Rolf. "Increased expression of matrix metalloproteinase 1 (MMP1) in 11 patients with patellar tendinosis." Acta Orthopaedica Scandinavica 73, no. 6 (December 2002): 658–62. http://dx.doi.org/10.3109/17453670209178031.

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Fu, Sai C., Barbara P. Chan, Wen Wang, Hon M. Pau, Kai M. Chan, and Christer G. Rolf. "Increased expression of matrix metalloproteinase 1 (MMP1) in 11 patients with patellar tendinosis." Acta Orthopaedica Scandinavica 73, no. 6 (December 1, 2002): 658–62. http://dx.doi.org/10.1080/000164702321039624.

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Wang, Yu, Danyang Zhao, Xiao Wei, Lin Ma, Jing Sheng, and Ping Lu. "PEGylated Polyethylenimine Derivative-Mediated Local Delivery of the shSmad3 Inhibits Intimal Thickening after Vascular Injury." BioMed Research International 2019 (July 29, 2019): 1–15. http://dx.doi.org/10.1155/2019/8483765.

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Intimal hyperplasia is a complex process which contributes to several clinical problems such as atherosclerosis and postangioplasty restenosis. Inhibition of Smad3 expression inhibits intimal thickening. Our previous study has modified biscarbamate cross-linked polyethylenimine derivative (PEI-Et) through PEGylation thus obtained polyethylene glycol-graft-polyethylenimine derivative (PEG-Et 1:1), which has lower cytotoxicity and higher gene transfection efficiency compared with PEI-Et. In this study, PEG-Et 1:1 was employed in Smad3 shRNA (shSmad3) delivery for preventing intimal hyperplasia after vascular injury. It was observed that PEG-Et 1:1 could condense shSmad3 gene into nanoparticles with particle size of 115–168 nm and zeta potential of 3–6 mV. PEG-Et 1:1 displayed remarkably lower cytotoxicity, higher transfection efficiency, and shRNA silencing efficiency than PEI-Et and PEI 25 kDa in vascular smooth muscle cells (VSMCs). Moreover, PEG-Et 1:1/shSmad3 polyplex treatment significantly inhibited collagen, matrix metalloproteinase 1 (MMP1), MMP2 and MMP9 expression, and upregulated tissue inhibitor of metalloproteinase 1 (TIMP1) expression both in vitro and in vivo. Furthermore, intravascular delivery of shSmad3 with PEG-Et 1:1 polyplex efficiently reduced Smad3 expression and inhibited intimal thickening 14 days after vascular injury. Ultimately, this study indicated that PEG-Et 1:1-mediated local delivery of shSmad3 is a promising strategy for preventing intimal thickening.

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Hui, Wang, Gary J. Litherland, Martina S. Elias, Gareth I. Kitson, Tim E. Cawston, Andrew D. Rowan, and David A. Young. "Leptin produced by joint white adipose tissue induces cartilage degradation via upregulation and activation of matrix metalloproteinases." Annals of the Rheumatic Diseases 71, no. 3 (November 9, 2011): 455–62. http://dx.doi.org/10.1136/annrheumdis-2011-200372.

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ObjectivesTo investigate the effect of leptin on cartilage destruction.MethodsCollagen release was assessed in bovine cartilage explant cultures, while collagenolytic and gelatinolytic activities in culture supernatants were determined by bioassay and gelatin zymography. The expression of matrix metalloproteinases (MMP) was analysed by real-time RT–PCR. Signalling pathway activation was studied by immunoblotting. Leptin levels in cultured osteoarthritic joint infrapatellar fat pad or peri-enthesal deposit supernatants were measured by immunoassay.ResultsLeptin, either alone or in synergy with IL-1, significantly induced collagen release from bovine cartilage by upregulating collagenolytic and gelatinolytic activity. In chondrocytes, leptin induced MMP1 and MMP13 expression with a concomitant activation of STAT1, STAT3, STAT5, MAPK (JNK, Erk, p38), Akt and NF-κB signalling pathways. Selective inhibitor blockade of PI3K, p38, Erk and Akt pathways significantly reduced MMP1 and MMP13 expression in chondrocytes, and reduced cartilage collagen release induced by leptin or leptin plus IL-1. JNK inhibition had no effect on leptin-induced MMP13 expression or leptin plus IL-1-induced cartilage collagen release. Conditioned media from cultured white adipose tissue (WAT) from osteoarthritis knee joint fat pads contained leptin, induced cartilage collagen release and increased MMP1 and MMP13 expression in chondrocytes; the latter being partly blocked with an anti-leptin antibody.ConclusionsLeptin acts as a pro-inflammatory adipokine with a catabolic role on cartilage metabolism via the upregulation of proteolytic enzymes and acts synergistically with other pro-inflammatory stimuli. This suggests that the infrapatellar fat pad and other WAT in arthritic joints are local producers of leptin, which may contribute to the inflammatory and degenerative processes in cartilage catabolism, providing a mechanistic link between obesity and osteoarthritis.

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Lelongt, Brigitte, Germain Trugnan, Gillian Murphy, and Pierre M. Ronco. "Matrix Metalloproteinases MMP2 and MMP9 Are Produced in Early Stages of Kidney Morphogenesis but Only MMP9 Is Required for Renal Organogenesis In Vitro." Journal of Cell Biology 136, no. 6 (March 24, 1997): 1363–73. http://dx.doi.org/10.1083/jcb.136.6.1363.

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We analyzed matrix metalloproteinase (MMP) production by 11-d embryonic mouse kidneys and the effects of these enzymes on subsequent renal organogenesis. In vivo, immunolocalization of metalloproteinases by laser scanning confocal microscopy and zymograms of kidney lysates showed that the mesenchyme of embryonic kidneys synthesized both MMP9 and MMP2 enzymes. In vitro, embryonic kidneys also secreted both enzymes when cultured in a medium devoid of hormone, growth factor, and serum for 24 h during which T-shaped branching of the ureter bud appeared. We then evaluated the role of MMP2 and MMP9 in kidney morphogenesis by adding anti-MMP2 or anti-MMP9 IgGs to the culture medium of 11-d kidneys for 24 or 72 h. Although it inhibited activity of the mouse enzyme, anti-MMP2 IgGs had no effect on kidney morphogenesis. In contrast, anti-MMP9 IgGs with enzyme-blocking activity impaired renal morphogenesis, in a concentration-dependent manner, by inhibiting T-shaped branching and further divisions of the ureter bud. This effect was irreversible, still observed after inductive events and reproduced by exogenous tissue inhibitor of metalloproteinase 1 (TIMP1), the natural inhibitor of MMP9. These data provide the first demonstration of MMP9 and MMP2 production in vivo by 11-d embryonic kidneys and further show that MMP9 is required in vitro for branching morphogenesis of the ureter bud.

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Koscica, Karen, Cande Ananth, and Sandra Reznik. "The effect of a matrix metalloproteinase-1 (MMP1) inhibitor on inflammation-mediated preterm delivery." American Journal of Obstetrics and Gynecology 189, no. 6 (December 2003): S67. http://dx.doi.org/10.1016/j.ajog.2003.10.028.

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Yassen, Mohy Eldin Abdel Fattah Abdel Atty, Olfat Ali Ibrahim Hammam, and Hazem Kamel Abdel-Aziz Mohamed Sarhan. "Expression of Matrix Metalloproteinase 1( MMP1 ) in Hepatocellular Carcinoma ( HCC ) : Immunohistochemical and Biochemical Studies." Egyptian Journal of Hospital Medicine 51 (April 2013): 289–99. http://dx.doi.org/10.12816/0000845.

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Yassen, Mohy Eldin abdel Fattah abdel Atty, Olfat Ali Ibrahim Hammam, and Hazem Kamel Abdel-Aziz Mohamed Sarhan. "Expression of Matrix Metalloproteinase 1(MMP1) in HepatoCellular Carcinoma (HCC): Immunohistochemical and Biochemical Studies." Egyptian Journal of Hospital Medicine 51, no. 1 (April 1, 2013): 289–99. http://dx.doi.org/10.21608/ejhm.2013.15979.

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Patra, Swagata, Parameswaran Saravanan, Bhaskar Das, Venkatesan Subramanian, and Sanjukta Patra. "Scaffold-based Screening and Molecular Dynamics Simulation Study to Identify Two Structurally Related Phenolic Compounds as Potent MMP1 Inhibitors." Combinatorial Chemistry & High Throughput Screening 23, no. 8 (November 2, 2020): 757–74. http://dx.doi.org/10.2174/1386207323666200428114216.

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Background: Matrix metalloproteinase 1 are zinc-dependent endopeptidases responsible for the controlled breakdown of the extracellular matrix resulting in the maintenance of homeostasis. Dysregulation of MMP1 leads to the progression of various pathological conditions like cancer, rheumatoid arthritis, cardiovascular disease, skin damage and fibrotic disorder. Thus, MMP1 inhibition is the potential drug target of many synthetic MMP1 inhibitors but lack of substrate specificity hinders their clinical applicability. Hence, inhibitors from natural products have gained widespread attention. Objective: The present study attempts screening of novel MMP1 inhibitors from the ZINC database based on experimentally reported natural inhibitors of MMP1 as a scaffold. Methods: Molecular docking study was performed with 19 experimentally reported natural inhibitors spanning across nine different classes followed by virtual screening using the selected compounds. The selected compounds were subjected to molecular dynamics simulation. Results: Twenty compounds were screened with a cut-off of -9.0 kcal/mol of predicted free energy of binding, which further converged to 6 hits after docking studies. After comparing the docking result of 6 screened hits, two best compounds were selected. ZINC02436922 had the best interaction with six hydrogen bond formation to a relatively confined region in the S1’site of MMP1 and -10.01 kcal/mol of predicted free energy of binding. ZINC03075557 was the secondbest compound with -9.57 kcal/mol predicted binding free energy. Molecular dynamics simulation of ZINC02436922 and ZINC03075557 corroborates docking study. Conclusion: This study indicated phenolic compounds ZINC02436922 and ZINC03075557 as potential MMP1 inhibitors.

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Inzitari, Domenico, Betti Giusti, Patrizia Nencini, Anna Maria Gori, Mascia Nesi, Vanessa Palumbo, Benedetta Piccardi, et al. "MMP9 Variation After Thrombolysis Is Associated With Hemorrhagic Transformation of Lesion and Death." Stroke 44, no. 10 (October 2013): 2901–3. http://dx.doi.org/10.1161/strokeaha.113.002274.

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Background and Purpose— Experimentally, matrix metalloproteinases (MMPs) play a detrimental role related to hemorrhagic transformation and severity of an ischemic brain lesion. Tissue-type plasminogen activator (tPA) enhances such effects. This study aimed to expand clinical evidence in this connection. Methods— We measured MMPs 1, 2, 3, 7, 8, 9, and tissue inhibitors of metalloproteinases 1, 2, 4 circulating level in blood taken before and 24 hours after tPA from 327 patients (mean age, 68.9±12.1 years; median National Institutes of Health Stroke Scale, 11) with acute ischemic stroke. Delta median values ([24 hours post tPA–pre tPA]/pre tPA) of each MMP or tissue inhibitors of metalloproteinase were analyzed across subgroups of patients undergoing symptomatic intracerebral hemorrhage, 3-month death, or 3-month modified Rankin Scale score 3 to 6. Results— Adjusting for major clinical determinants, only matrix metalloproteinase-9 variation proved independently associated with death (odds ratio [95% confidence interval], 1.58 [1.11–2.26]; P =0.045) or symptomatic intracerebral hemorrhage (odds ratio [95% confidence interval], 1.40 [1.02–1.92]; P =0.049). Both matrix metalloproteinase-9 and tissue inhibitors of metalloproteinase-4 changes were correlated with baseline, 24 hours, and 7 days National Institutes of Health Stroke Scale (Spearman P from <0.001 to 0.040). Conclusions— Our clinical evidence corroborates the detrimental role of matrix metalloproteinase-9 during ischemic stroke treated with thrombolysis, and prompts clinical trials testing agents antagonizing its effects.

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Li, Chuan, Zhi Peng, You Zhou, Yongyue Su, Pengfei Bu, Xuhan Meng, Bo Li, and Yongqing Xu. "Comprehensive analysis of pathological changes in hip joint capsule of patients with developmental dysplasia of the hip." Bone & Joint Research 10, no. 9 (September 1, 2021): 558–70. http://dx.doi.org/10.1302/2046-3758.109.bjr-2020-0421.r2.

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Aims Developmental dysplasia of the hip (DDH) is a complex musculoskeletal disease that occurs mostly in children. This study aimed to investigate the molecular changes in the hip joint capsule of patients with DDH. Methods High-throughput sequencing was used to identify genes that were differentially expressed in hip joint capsules between healthy controls and DDH patients. Biological assays including cell cycle, viability, apoptosis, immunofluorescence, reverse transcription polymerase chain reaction (RT-PCR), and western blotting were performed to determine the roles of the differentially expressed genes in DDH pathology. Results More than 1,000 genes were differentially expressed in hip joint capsules between healthy controls and DDH. Both gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that extracellular matrix (ECM) modifications, muscle system processes, and cell proliferation were markedly influenced by the differentially expressed genes. Expression of Collagen Type I Alpha 1 Chain (COL1A1), COL3A1, matrix metalloproteinase-1 (MMP1), MMP3, MMP9, and MMP13 was downregulated in DDH, with the loss of collagen fibres in the joint capsule. Expression of transforming growth factor beta 1 (TGF-β1) was downregulated, while that of TGF-β2, Mothers against decapentaplegic homolog 3 (SMAD3), and WNT11 were upregulated in DDH, and alpha smooth muscle actin (αSMA), a key myofibroblast marker, showed marginal increase. In vitro studies showed that fibroblast proliferation was suppressed in DDH, which was associated with cell cycle arrest in G0/G1 and G2/M phases. Cell cycle regulators including Cyclin B1 (CCNB1), Cyclin E2 (CCNE2), Cyclin A2 (CCNA2), Cyclin-dependent kinase 1 (CDK1), E2F1, cell division cycle 6 (CDC6), and CDC7 were downregulated in DDH. Conclusion DDH is associated with the loss of collagen fibres and fibroblasts, which may cause loose joint capsule formation. However, the degree of differentiation of fibroblasts to myofibroblasts needs further study. Cite this article: Bone Joint Res 2021;10(9):558–570.

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Supp, Dorothy M., Kevin L. McFarland, Jennifer M. Hahn, and Kelly A. Combs. "140 Alpha-Mangostin Inhibits Proliferation, Promotes Apoptosis, and Modulates Fibrotic Gene Expression in Normal and Keloid Fibroblasts In Vitro." Journal of Burn Care & Research 42, Supplement_1 (April 1, 2021): S93—S94. http://dx.doi.org/10.1093/jbcr/irab032.144.

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Abstract Introduction Keloids are disfiguring lesions that result from an abnormal wound healing process. Despite the availability of numerous therapeutic options, keloids remain challenging to treat and often recur after therapy. α-Mangostin, a natural xanthone isolated from the fruit of the Mangosteen tree, has been used for centuries in many Southeast Asian nations for medicinal purposes, and has gained attention more recently due to its anti-inflammatory, antimicrobial, and antioxidant properties, with numerous studies suggesting possible anticarcinogenic activities. Hypothetically, α-mangostin may have therapeutic value for keloid suppression. To investigate this hypothesis, the effects of α-mangostin on fibroblast proliferation, apoptosis, and gene expression in vitro were analyzed. Methods Dermal fibroblasts were isolated and cultured from normal human skin and excised keloid lesions (3 donors each), and were treated with multiple doses (0–10 µm) of α-mangostin in vitro. Proliferation was measured using an MTT assay, gene expression was measured using quantitative real-time PCR (qPCR), and protein levels in culture media were measured by enzyme-linked immunosorbent assay (ELISA). Apoptosis was assessed by measuring expression of C/EBP homologous protein (CHOP), which mediates endoplasmic reticulum stress-induced apoptosis, by qPCR. Results Dose-dependent decreases in proliferation of keloid and normal fibroblasts were observed following treatment with α-mangostin. The α-mangostin treated fibroblasts displayed significantly increased expression of CHOP, indicating increased apoptosis. In addition, numerous changes in gene expression were observed in α-mangostin-treated keloid fibroblasts, including decreased expression of collagen type I alpha 1 chain (COL1A1) and increased expression of matrix metalloproteinase 1 (MMP1), MMP3, and MMP13. Secretion of pro-collagen I was decreased, and secretion of MMP1 and MMP3 proteins were increased, in α-mangostin-treated fibroblasts. Conclusions The results suggest that α-mangostin may exhibit antiproliferative, proapoptotic, and antifibrotic activities in keloid and normal fibroblasts.

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Olmos-Zuñiga, J. Raúl, Matilde Baltazares-Lipp, Claudia Hernández-Jiménez, Rogelio Jasso-Victoria, Miguel Gaxiola-Gaxiola, Mariana Silva-Martínez, Marco Antonio Iñiguez-García, et al. "Treatment with Hyaluronic Acid and Collagen-Polyvinylpyrrolidone Improves Extracellular Matrix Assembly for Scarring after Tracheal Resection." BioMed Research International 2020 (August 27, 2020): 1–15. http://dx.doi.org/10.1155/2020/3964518.

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Treatment of tracheal stenosis is occasionally performed in combination with wound healing modulators to manipulate new extracellular matrix (ECM) formation and prevent fibrosis. Hyaluronic acid (HA) and collagen-polyvinylpyrrolidone (collagen-PVP) decrease fibrosis in experimental tracheal healing. However, they have not been used clinically as their effect on ECM components, which modify tracheal scarring, has not been described. Objective. To evaluate the effect of the application of HA, collagen-PVP, a mixture of HA and collagen-PVP (HA+collagen-PVP), and mitomycin C on the expression of decorin, matrix metalloproteinase 1 (MMP1), and MMP9, as well as the type of collagen and deposits formed in the scar after resection and end-to-end anastomosis (REEA) of the cervical trachea using an experimental model. Materials and Methods. Thirty dogs underwent REEA of the cervical trachea and were treated with different wound healing modulators: group I (n=6), control; group II (n=6), HA; group III (n=6), collagen-PVP; group IV (n=6), HA+collagen-PVP; and group V (n=6), mitomycin C. The dogs were evaluated clinically and endoscopically for 4 weeks. Subsequently, macroscopic and microscopic changes, expression of ECM proteins, and collagen deposition in tracheal scars were analysed. Results. Groups II, III, and IV showed reduced endoscopic, macroscopic, and microscopic inflammation, improved neovascularization, high decorin expression (p<0.01, analysis of variance (ANOVA)), and moderate expression of MMP1 (p<0.003, ANOVA) and type I and III collagen (p<0.05, Kruskal–Wallis). Groups IV and V developed fewer collagen deposits (p<0.001, ANOVA). Conclusion. Treatment with HA and collagen-PVP improved post-REEA healing by increasing neovascularization, stimulating the expression of decorin, and regulating the expression of MMP1, as well as type I and III collagen and their deposition.

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Lefebvre-Lavoie, Josiane, Jacques G. Lussier, and Christine L. Theoret. "Profiling of differentially expressed genes in wound margin biopsies of horses using suppression subtractive hybridization." Physiological Genomics 22, no. 2 (July 14, 2005): 157–70. http://dx.doi.org/10.1152/physiolgenomics.00018.2005.

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Disturbed gene expression may disrupt the normal process of repair and lead to pathological situations resulting in excessive scarring. To prevent and treat impaired healing, it is necessary to first define baseline gene expression during normal repair. The objective of this study was to compare gene expression in normal intact skin (IS) and wound margin (WM) biopsies using suppression subtractive hybridization (SSH) to identify genes differentially expressed during wound repair in horses. Tissue samples included both normal IS and biopsies from 7-day-old wounds. IS cDNAs were subtracted from WM cDNAs to establish a subtracted (WM-IS) cDNA library; 226 nonredundant cDNAs were identified. Detection of genes previously shown to be expressed 7 days after trauma, including the pro-α2-chain of type 1 pro-collagen (COL1A2), annexin A2, the pro-α3-chain of type 6 pro-collagen, β-actin, fibroblast growth factor 7, laminin receptor 1, matrix metalloproteinase 1 (MMP1), secreted protein acidic cystein rich, and tissue inhibitor of metalloproteinase 2, supported the validity of the experimental design. A RT-PCR assay confirmed an increase or induction of the cDNAs of specific genes (COL1A2, MMP1, dermatan sulfate proteoglycan 2, cluster differentiation 68, cluster differentiation 163, and disintegrin and metalloproteinase domain 9) within wound biopsies. Among these, COL1A2 and MMP1 had previously been documented in horses; 68.8% of the cDNAs had not previously been attributed a role during wound repair, of which spermidine/spermine- N-acetyltransferase, serin proteinase inhibitor B10, and sorting nexin 9 were highly expressed and whose known functions in other processes made them potential candidates in regulating the proliferative response to wounding. In conclusion, we identified novel genes that are differentially expressed in equine wound biopsies and that may modulate repair. Future experiments must correlate changes in mRNA levels for precise molecules with spatiotemporal protein expression within tissues.

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Chen, Jen-Liang, Chung-Yu Lai, Tsung-Ho Ying, Chiao-Wen Lin, Pei-Han Wang, Fang-Jung Yu, Chung-Jung Liu, and Yi-Hsien Hsieh. "Modulating the ERK1/2–MMP1 Axis through Corosolic Acid Inhibits Metastasis of Human Oral Squamous Cell Carcinoma Cells." International Journal of Molecular Sciences 22, no. 16 (August 11, 2021): 8641. http://dx.doi.org/10.3390/ijms22168641.

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Corosolic acid (CA; 2α-hydroxyursolic acid) is a natural pentacyclic triterpenoid with antioxidant, antitumour and antimetastatic activities against various tumour cells during tumourigenesis. However, CA’s antitumour effect and functional roles on human oral squamous cell carcinoma (OSCC) cells are utterly unknown. In this study, our results demonstrated that CA significantly exerted an inhibitory effect on matrix metalloproteinase (MMP)1 expression, cell migration and invasion without influencing cell growth or the cell cycle of human OSCC cells. The critical role of MMP1 was confirmed using the GEPIA database and showed that patients have a high expression of MMP1 and have a shorter overall survival rate, confirmed on the Kaplan–Meier curve assay. In the synergistic inhibitory analysis, CA and siMMP1 co-treatment showed a synergically inhibitory influence on MMP1 expression and invasion of human OSCC cells. The ERK1/2 pathway plays an essential role in mediating tumour progression. We found that CA significantly inhibits the phosphorylation of ERK1/2 dose-dependently. The ERK1/2 pathway played an essential role in the CA-mediated downregulation of MMP1 expression and in invasive motility in human OSCC cells. These findings first demonstrated the inhibitory effects of CA on OSCC cells’ progression through inhibition of the ERK1/2–MMP1 axis. Therefore, CA might represent a novel strategy for treating OSCC.

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Lee, Jaemin, Dong-Hee Kim, Eun-Woo Kim, Hyun Ju Kwon, Byung Woo Kim, Jae-Hyon Cho, Hyun-Joo Kim, and Tae Hoon Kim. "Matrix metalloproteinase-1 suppression and type-1 procollagen synthesis promoting effects of Uncaria gambir." Korean Journal of Food Preservation 24, no. 1 (February 2017): 93–99. http://dx.doi.org/10.11002/kjfp.2017.24.1.93.

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Cheng, Xiaoyun, Wenke Gao, Yongyan Dang, Xia Liu, Yujuan Li, Xu Peng, and Xiyun Ye. "Both ERK/MAPK and TGF-Beta/Smad Signaling Pathways Play a Role in the Kidney Fibrosis of Diabetic Mice Accelerated by Blood Glucose Fluctuation." Journal of Diabetes Research 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/463740.

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Abstract (sommario):

Background. The notion that diabetic nephropathy is the leading cause of renal fibrosis prompted us to investigate the effects of blood glucose fluctuation (BGF) under high glucose condition on kidney in the mice.Methods. The diabetic and BGF animal models were established in this study. Immunohistochemistry, Western blot, and RT-PCR analysis were applied to detect the expression of type I collagen, matrix metalloproteinase-1 (MMP1), metalloproteinase inhibitor 1 (TIMP1), transforming growth factor beta 1 (TGF-β1), phosphorylated-ERK, p38, smad2/3, and Akt.Results. BGF treatment increased type I collagen synthesis by two times compared with the control. The expression of MMP1 was reduced markedly while TIMP1 synthesis was enhanced after BGF treatment. ERK phosphorylation exhibits a significant increase in the mice treated with BGF. Furthermore, BGF can markedly upregulate TGF-β1 expression. The p-smad2 showed 2-fold increases compared with the only diabetic mice. However, p-AKT levels were unchanged after BGF treatment.Conclusions. These data demonstrate that BGF can accelerate the trend of kidney fibrosis in diabetic mice by increasing collagen production and inhibiting collagen degradation. Both ERK/MAPK and TGF-β/smad signaling pathways seem to play a role in the development of kidney fibrosis accelerated by blood glucose fluctuation.

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Li, Zhen, Hongzhou Ge, Yong-Gang Xie, Guang-Ying Xie, and Chao Lv. "Matrix Metalloproteinase-1 (MMP1) Polymorphism is Associated with Lowered Risk of Nasopharyngeal Carcinoma in Asian Population." Cell Biochemistry and Biophysics 71, no. 2 (October 14, 2014): 999–1004. http://dx.doi.org/10.1007/s12013-014-0299-4.

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Lin, Jiayu, Chaowen Deng, Yanzhong Peng, Jie Zheng, Liya Wei, Yu Shi, Zhenghua Gong, and Guoxin Hu. "Dynamic Changes in MMP1 and TIMP1 in the Antifibrotic Process of Dahuang Zhechong Pill in Rats with Liver Fibrosis." Open Chemistry 17, no. 1 (June 1, 2019): 346–56. http://dx.doi.org/10.1515/chem-2019-0041.

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AbstractOn the basis of carbon tetrachloride (CCl4)induced liver fibrosis in rats, this study aims to investigate the dynamic changes in matrix metalloproteinase 1 (MMP1) and the tissue inhibitor of metalloproteinase 1 (TIMP1) in the antifibrotic process of Dahuang Zhechong Pill (DHZCP). A total of 50 male Sprague Dawley rats, aged 8 weeks, were randomly divided into 3 groups: the control group, the model group (the group treated with CCl4), and the treatment group (the group treated with CCl4 and DHZCP). Rats were sacrificed at Weeks 4 and 8. Liver tissues were separated for RNA sequencing and bioinformatics analysis. Real-time PCR, Western blot analysis, and histological staining were conducted to confirm the gene expression and pathological change in liver tissues. Compared with control group, rats in model group showed poor mental state and slow weight gain. The liver tissues of the rats in the model group exhibited a damaged hepatic lobule structure, fibrous connective tissue hyperplasia, and inflammatory cell infiltration among the hyperplastic tissues. DHZCP could significantly improve the appearance of rats and alleviate CCl4-induced fibrosis. Compared to model group, 798 differentially expressed mRNAs were found in the treatment group, of which 120 were up-regulated and 678 were down-regulated. Differentially expressed mRNAs between the CCl4-induced group and the DHZCP-treated group were mainly focused on the following KEGG pathways: focal adhesion, phagosome, tight junction, and ECM–receptor interactions. Relative to those in the control group, MMP1 was downregulated, whereas, TIMP1 and Col1A1 were upregulated in the CCl4-induced group at Weeks 4 and 8. DHZCP could reverse MMP1, TIMP1, and Col1A1 expression.DHZCP protects against liver injury and exerts an antifibrotic effect on liver fibrosis induced by CCl4 in rats. Its mechanism may be related to the upregulation of MMP1, downregulation of TIMP1, and promotion of collagen degradation.

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El-Sheikh Ali, Hossam, Kirsten E. Scoggin, Rebecca Ruby, Alan Loynachan, Yatta Boakari, Claudia Fernandes, Pouya Dini, et al. "Equine cervical remodeling during placentitis and the prepartum period: a transcriptomic approach." Reproduction 161, no. 6 (June 1, 2021): 603–21. http://dx.doi.org/10.1530/rep-21-0008.

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Cervical remodeling is a critical component in both term and preterm labor in eutherian mammals. However, the molecular mechanisms underlying cervical remodeling remain poorly understood in the mare. The current study compared the transcriptome of the equine cervix (cervical mucosa (CM) and stroma (CS)) during placentitis (placentitis group, n = 5) and normal prepartum mares (prepartum group, n = 3) to normal pregnant mares (control group, n = 4). Transcriptome analysis identified differentially expressed genes (DEGs) during placentitis (5310 in CM and 907 in CS) and during the normal prepartum period (189 in CM and 78 in CS). Our study revealed that cervical remodeling during placentitis was dominated by inflammatory signaling as reflected by the overrepresented toll-like receptor signaling, interleukin signaling, T cell activation, and B cell activation pathways. These pathways were accompanied by upregulation of several proteases, including matrix metalloproteinases (MMP1, MMP2, and MMP9), cathepsins (CTSB, CTSC, and CTSD) and a disintegrin and metalloproteinase with thrombospondin type 1 motifs (ADAMTS1, ADAMTS4, and ADAMTS5), which are crucial for degradation of cervical collagens during remodeling. Cervical remodeling during placentitis was also associated with upregulation of water channel-related transcripts (AQP9 and RLN), angiogenesis-related transcripts (NOS3, ENG1, THBS1, and RAC2), and aggrecan (ACAN), a hydrophilic glucosaminoglycan, with subsequent cervical hydration. The normal prepartum cervix was associated with upregulation of ADAMTS1, ADAMTS4, NOS3 and THBS1, which might reflect an early stage of cervical remodeling taking place in preparation for labor. In conclusion, our findings revealed the possible key regulators and mechanisms underlying equine cervical remodeling during placentitis and the normal prepartum period.

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Kim, Young Joo, and Hwa Jun Cha. "Inonotus obliquus Extracts Decreased Expression of MMP1 mRNA via JNK-AP-1 Axis." Cosmetics 7, no. 2 (May 18, 2020): 36. http://dx.doi.org/10.3390/cosmetics7020036.

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Inonotus obliquus, which is parasitic on birch and other trees, is a fungus in the family Hymenochaetaceae. In this study, we investigated whether Inonotus obliquus extracts used in traditional medicine were decreased in the expression of matrix metalloproteinases-1 (MMP-1) in the normal human dermal fibroblasts. As shown in our results, extracts of Inonotus obliquus decreased MMP1 expression in oxidative stress-exposed normal human dermal fibroblasts. Additionally, Inonotus obliquus extracts decreased AP-1 transcriptional activity and phospho-JNK in oxidative stress-exposed normal human dermal fibroblasts. Oxidative stress mediated the elevation of MMP1 mRNA expression and was well regulated by the JNK-AP-1 axis. Therefore, the results suggest that Inonotus obliquus extracts decreased MMP1 mRNA expression by regulating JNK-AP-1 axis. Additionally, Inonotus obliquus extracts have the potential to reduce collagen destruction and the formation of wrinkles and to be used as a cosmetic ingredient.

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Li, Ming, Akitake Mukasa, Maria del-Mar Inda, Jianhua Zhang, Lynda Chin, Webster Cavenee, and Frank Furnari. "Guanylate binding protein 1 is a novel effector of EGFR-driven invasion in glioblastoma." Journal of Experimental Medicine 208, no. 13 (December 12, 2011): 2657–73. http://dx.doi.org/10.1084/jem.20111102.

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Although GBP1 (guanylate binding protein 1) was among the first interferon-inducible proteins identified, its function is still largely unknown. Epidermal growth factor receptor (EGFR) activation by amplification or mutation is one of the most frequent genetic lesions in a variety of human tumors. These include glioblastoma multiforme (GBM), which is characterized by independent but interrelated features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenesis. In this study, we show that EGFR activation promoted GBP1 expression in GBM cell lines through a signaling pathway involving Src and p38 mitogen-activated protein kinase. Moreover, we identified YY1 (Yin Yang 1) as the downstream transcriptional regulator regulating EGFR-driven GBP1 expression. GBP1 was required for EGFR-mediated MMP1 (matrix metalloproteinase 1) expression and glioma cell invasion in vitro. Although deregulation of GBP1 expression did not affect glioma cell proliferation, overexpression of GBP1 enhanced glioma cell invasion through MMP1 induction, which required its C-terminal helical domain and was independent of its GTPase activity. Reducing GBP1 levels by RNA interference in invasive GBM cells also markedly inhibited their ability to infiltrate the brain parenchyma of mice. GBP1 expression was high and positively correlated with EGFR expression in human GBM tumors and cell lines, particularly those of the neural subtype. Together, these findings establish GBP1 as a previously unknown link between EGFR activity and MMP1 expression and nominate it as a novel potential therapeutic target for inhibiting GBM invasion.

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Chellaiah, Meenakshi A., and Tao Ma. "Membrane Localization of Membrane Type 1 Matrix Metalloproteinase by CD44 Regulates the Activation of Pro-Matrix Metalloproteinase 9 in Osteoclasts." BioMed Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/302392.

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CD44, MT1-MMP, and MMP9 are implicated in the migration of osteoclast and bone resorption. This study was designed to determine the functional relationship between CD44 and MT1-MMP in the activation of pro-MMP9. We used osteoclasts isolated from wild-type and CD44-null mice. Results showed that MT1-MMP is present in multiple forms with a molecular mass ~63, 55, and 45 kDa in the membrane of wild-type osteoclasts. CD44-null osteoclasts demonstrated a 55 kDa active MT1-MMP form in the membrane and conditioned medium. It failed to activate pro-MMP9 because TIMP2 binds and inhibits this MT1-MMP (~55 kDa) in CD44-null osteoclasts. The role of MT1-MMP in the activation of pro-MMP9, CD44 expression, and migration was confirmed by knockdown of MT1-MMP in wild-type osteoclasts. Although knockdown of MMP9 suppressed osteoclast migration, it had no effects on MT1-MMP activity or CD44 expression. These results suggest that CD44 and MT1-MMP are directly or indirectly involved in the regulation of pro-MMP9 activation. Surface expression of CD44, membrane localization of MT1-MMP, and activation of pro-MMP9 are the necessary sequence of events in osteoclast migration.

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Chen, Guobing, Dandan Ge, Bizhen Zhu, Huixuan Shi, and Qilin Ma. "Upregulation of matrix metalloproteinase 9 (MMP9)/tissue inhibitor of metalloproteinase 1 (TIMP1) and MMP2/TIMP2 ratios may be involved in lipopolysaccharide-induced acute lung injury." Journal of International Medical Research 48, no. 4 (April 2020): 030006052091959. http://dx.doi.org/10.1177/0300060520919592.

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Objective This study aimed to examine the changes and significance of matrix metalloproteinase 9 (MMP9), MMP2, tissue inhibitor of metalloproteinase 1 (TIMP1), and TIMP2 in rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods Wistar rats were randomly divided into a control group (injected with saline) and an ALI group (injected with LPS), then subdivided into four time points (2, 6, 12, and 24 hours). Serum tumor necrosis factor alpha and interleukin-6 levels were detected by ELISA to investigate the inflammatory reaction after LPS injection. The degree of ALI was determined by hematoxylin–eosin staining of lung tissue, the lung wet/dry weight ratio, and pulmonary permeability index. Changes in lung MMP and TIMP protein and mRNA levels were detected by western blotting and quantitative real-time polymerase chain reaction. Results Changes in the ratios of MMP9/TIMP1 and MMP2/TIMP2 were consistent with and strongly positively associated with the lung wet/dry weight ratio, the pulmonary permeability index, and serum tumor necrosis factor alpha and interleukin-6 levels in the ALI group. Conclusion ALI induced by LPS may be related to upregulation of MMP9/TIMP1 and MMP2/TIMP2 ratios.

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Verma, Archana, Aneesh Shrivastava, and Rama D. Mittal. "Association of Matrix Metalloproteinase 1 and 3 (MMP1 and MMP3) gene polymorphisms with susceptibility to ESRD risk in North Indian population." Molecular Cytogenetics 7, Suppl 1 (2014): P30. http://dx.doi.org/10.1186/1755-8166-7-s1-p30.

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Sauter, W., A. Rosenberger, L. Beckmann, M. Timofeeva, K. Mittelstrass, T. Illig, J. Chang-Claude, H. E. Wichmann, H. Bickeböller, and A. Risch. "Case-control study of genetic susceptibility in early onset lung cancer: Investigation of Matrix Metalloproteinase-1 (MMP1)." European Journal of Cancer Supplements 6, no. 9 (July 2008): 205. http://dx.doi.org/10.1016/s1359-6349(08)71903-7.

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Wang, Lijie, and Beihua Kong. "Analysis of the Association of Matrix Metalloproteinase-1 Gene Promoter (rs1799750) Polymorphism and Risk of Ovarian Cancer." International Journal of Gynecologic Cancer 25, no. 6 (July 2015): 961–67. http://dx.doi.org/10.1097/igc.0000000000000463.

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Abstract (sommario):

ObjectiveStudies investigating the association betweenmatrix metalloproteinase-1(MMP1) gene promoter 1607–base pair (bp) polymorphism and ovarian cancer risk have yielded conflicting results.MethodsWe therefore carried out a meta-analysis of 754 ovarian cancer cases and 1184 controls from 5 published case-control studies. The strength of the association betweenMMP11607-bp polymorphism and ovarian cancer susceptibility was calculated using pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs).ResultsThe results suggest that no statistically significant associations exist betweenMMP11607-bp polymorphisms and ovarian cancer risk in all 4 genetic models (2G2G vs 1G1G: OR, 1.08; 95% CI, 0.81–1.43;P= 0.23; 1G2G vs 1G1G: OR, 1.06; 95% CI, 0.82–1.36;P= 0.15; 1G2G + 2G2G vs 1G1G: OR, 1.05; 95% CI, 0.83–1.34;P= 0.16; 2G2G vs 1G1G + 1G2G: OR, 0.98; 95% CI, 0.80–1.20;P= 0.84).ConclusionsIn summary, this meta-analysis showed that theMMP11607-bp polymorphism is not associated with ovarian cancer risk.

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Gömöri, Kamilla, Tamara Szabados, Éva Kenyeres, Judit Pipis, Imre Földesi, Andrea Siska, György Dormán, Péter Ferdinandy, Anikó Görbe, and Péter Bencsik. "Cardioprotective Effect of Novel Matrix Metalloproteinase Inhibitors." International Journal of Molecular Sciences 21, no. 19 (September 23, 2020): 6990. http://dx.doi.org/10.3390/ijms21196990.

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Background: We recently developed novel matrix metalloproteinase-2 (MMP-2) inhibitor small molecules for cardioprotection against ischemia/reperfusion injury and validated their efficacy in ischemia/reperfusion injury in cardiac myocytes. The aim of the present study was to test our lead compounds for cardioprotection in vivo in a rat model of acute myocardial infarction (AMI) in the presence or absence of hypercholesterolemia, one of the major comorbidities affecting cardioprotection. Methods: Normocholesterolemic adult male Wistar rats were subjected to 30 min of coronary occlusion followed by 120 min of reperfusion to induce AMI. MMP inhibitors (MMPI)-1154 and -1260 at 0.3, 1, and 3 µmol/kg, MMPI-1248 at 1, 3, and 10 µmol/kg were administered at the 25th min of ischemia intravenously. In separate groups, hypercholesterolemia was induced by a 12-week diet (2% cholesterol, 0.25% cholic acid), then the rats were subjected to the same AMI protocol and single doses of the MMPIs that showed the most efficacy in normocholesterolemic animals were tested in the hypercholesterolemic animals. Infarct size/area at risk was assessed at the end of reperfusion in all groups by standard Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining, and myocardial microvascular obstruction (MVO) was determined by thioflavine-S staining. Results: MMPI-1154 at 1 µmol/kg, MMPI-1260 at 3 µmol/kg and ischemic preconditioning (IPC) as the positive control reduced infarct size significantly; however, this effect was not seen in hypercholesterolemic animals. MVO in hypercholesterolemic animals decreased by IPC only. Conclusions: This is the first demonstration that MMPI-1154 and MMPI-1260 showed a dose-dependent infarct size reduction in an in vivo rat AMI model; however, single doses that showed the most efficacy in normocholesterolemic animals were abolished by hypercholesterolemia. The further development of these promising cardioprotective MMPIs should be continued with different dose ranges in the study of hypercholesterolemia and other comorbidities.

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Yuan, Yuan, Hisao Naito, Kazuya Kitamori, Sayuki Hashimoto, Tomomi Asano, and Tamie Nakajima. "The antihypertensive agent hydralazine reduced extracellular matrix synthesis and liver fibrosis in nonalcoholic steatohepatitis exacerbated by hypertension." PLOS ONE 15, no. 12 (December 14, 2020): e0243846. http://dx.doi.org/10.1371/journal.pone.0243846.

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Hypertension is an important risk factor for nonalcoholic steatohepatitis. We have previously demonstrated that hypertensive rats fed a high fat and cholesterol (HFC) diet incurred a more severe hepatic inflammatory response and fibrosis. Here we investigated the role of hypertension in NASH by comparing HFC-induced hepatic fibrogenesis between spontaneously hypertensive rats (SHRs) and their normotensive Wistar Kyoto counterpart. Compared to the counterpart, the HFC diet led to stronger aggregation of CD68-positive macrophages in SHRs. HFC feeding also resulted in significantly higher upregulation of the fibrosis-related gene alpha-smooth muscle actin in SHR. The HFC diet induced higher overexpression of serum tissue inhibitor of metalloproteinase-1 (TIMP1) and greater suppression of matrix metalloproteinase-2 (MMP2):TIMP1, MMP8:TIMP1, and MMP9:TIMP1 ratios, as a proxy of the activities of these MMPs in SHR. Administration of the antihypertensive agent hydralazine to SHRs significantly ameliorated HFC-induced liver fibrosis; it suppressed the aggregation of CD68-positive macrophages and the upregulation of platelet-derived growth factor receptor beta, and collagen, type 1, alpha-1 chain. In conclusion, a hypertensive environment exacerbated the hepatic fibrogenetic effects of the HFC diet; while the effects were partially reversed by the antihypertensive agent hydralazine. Our data suggest that antihypertensive drugs hold promise for treating NASH exacerbated by hypertension.

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Costa, L., I. Alho, A. G. Oliveira, M. Bicho, R. Carvalho, A. Fernandes, S. Ali, K. Leitzel, L. Demers, and A. Lipton. "309 POSTER Serum matrix metalloproteinase 1 (MMP1) as a prognostic marker in bone metastases (BM) treated with bisphosphonates." European Journal of Cancer Supplements 5, no. 4 (September 2007): 59. http://dx.doi.org/10.1016/s1359-6349(07)70327-0.

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Kang, Wesuk, Dabin Choi, and Taesun Park. "Dietary Suberic Acid Protects Against UVB-Induced Skin Photoaging in Hairless Mice." Nutrients 11, no. 12 (December 4, 2019): 2948. http://dx.doi.org/10.3390/nu11122948.

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Abstract (sommario):

Ultraviolet (UV) radiation is a major cause of skin photoaging, which is mainly characterized by dryness and wrinkle formation. In the current study, we investigated the anti-photoaging effects of dietary suberic acid, a naturally occurring photochemical, using UVB-irradiated hairless mice. Mice were exposed to UVB three times weekly and fed diets containing three different suberic acid concentrations (0.05%, 0.1% and 0.2%) for 10 weeks. It was found that suberic acid inhibited UVB-induced skin dryness, wrinkle formation, and epidermal thickness in hairless mice. In parallel with phenotypic changes, suberic acid attenuated UVB-induced matrix metalloproteinase (MMP) genes (MMP1a, MMP1b, MMP3, and MMP9), while accelerating collagen genes including collagen type I alpha 1 chain (COL1A1), COL1A2, and COL3A1 and hyaluronic acid synthases genes (HAS1, HAS2 and HAS3). We further demonstrated that suberic acid upregulated the molecules involved in the transforming growth factor–β (TGF-β)/SMAD pathway, but downregulated the molecules participating in the mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) signaling in UVB-irritated hairless mice. Collectively, we propose that suberic acid may be a promising agent for treating skin photoaging.

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