{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T21:05:19Z","timestamp":1789679119273,"version":"4.0.1"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2019,5,6]],"date-time":"2019-05-06T00:00:00Z","timestamp":1557100800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"High-level Health Technical Talents Training Project in Beijing Health System","award":["12015B2003"],"award-info":[{"award-number":["12015B2003"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>This study was aimed to unveil micro RNA (miRNA) expression profiles in myocardial ischemia\u2010reperfusion (MI\/R) rats and explore whether and how dysregulated miRNAs were involved in the initiation and progression of MI\/R in a calcium\u2010dependent manner.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method and Results<\/jats:title><jats:p>Rat model of MI\/R was established and cardiomyocytes isolated from neonatal rats\u00a0cardiomyocytes were induced. Both miRNA and messenger RNA expression profiles were analyzed by Microarray. Quantitative reverse\u2010transcription polymerase chain reaction, immunoblotting, bioinformatics analysis, dual\u2010luciferase reporter gene assay, hematoxylin and eosin, Evans blue, and triphenyl tetrazolium chloride were also used in this study. Serum concentrations of myocardial enzymes (phosphocreatine kinase [CK], creatine kinase [CK\u2010MB], lactate dehydrogenase [LDH]), cardiomyocytes loadage of Ca<jats:sup>2+<\/jats:sup>, as well as the expression level of inositol 1,4,5\u2010trisphosphate receptors (IP3R) and sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup>\u2010ATPase 2a (SERCA2a) were measured, respectively. Effects of upregulation or downregulation of miR\u2010202\u20105p or <jats:italic>Trpv2<\/jats:italic> on these indicators were investigated in vivo and in vitro. In MI\/R rats and hypoxia\/reoxygenation\u2010induced NCMs, miR\u2010202\u20105p was downregulated, while <jats:italic>Trpv2<\/jats:italic> was upregulated. <jats:italic>Trpv2<\/jats:italic> was a promising target of miR\u2010202\u20105p and negatively regulated by miR\u2010202\u20105p. Upregulation of miR\u2010202\u20105p or downregulation of <jats:italic>Trpv2<\/jats:italic> significantly reduced the serum concentration of myocardial enzymes, as well as cardiomyocyte\u2010produced reactive oxygen species, but inhibition of miR\u2010202\u20105p or overexpression of <jats:italic>Trpv2<\/jats:italic> brought the worsening situation for these indicators. Besides, upregulation of miR\u2010202\u20105p upregulation or downregulation of <jats:italic>Trpv2<\/jats:italic> also inhibited Ca<jats:sup>2+<\/jats:sup> overload in cardiomyocytes, accompanied with the increase of SERCA2a and suppression of IP3R. The reduced damage degree and infarct size in myocardial tissue were contrarily worsened by miR\u2010202\u20105p inhibitor.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Overexpression of miR\u2010202\u20105p or downregulation of its downstream <jats:italic>Trpv2<\/jats:italic> presented the cardioprotective effects to MI\/R rats.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.28641","type":"journal-article","created":{"date-parts":[[2019,5,7]],"date-time":"2019-05-07T03:45:08Z","timestamp":1557200708000},"page":"13680-13693","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["miR\u2010202\u20105p protects rat against myocardial ischemia reperfusion injury by downregulating the expression of <i>Trpv2<\/i> to attenuate the Ca<sup>2+<\/sup> overload in cardiomyocytes"],"prefix":"10.1002","volume":"120","author":[{"given":"Yanbing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Cardiology Beijing Chao\u2010Yang Hospital, Capital Medical University Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology Beijing Chao\u2010Yang Hospital, Capital Medical University Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ou","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Beijing Tsinghua Chang Gung Hospital, Tsinghua University Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaonan","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Cardiology Beijing Chao\u2010Yang Hospital, Capital Medical University Beijing 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