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MicroRNAs (miRs) is a novel class of regulators of cardiovascular diseases such as MI. This study aimed to explore the role of miR-98 in MI and its underlying mechanisms. We found that miR-98 was downregulated both in infarcted and ischemic myocardium of MI mice as well as H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated neonatal rat ventricular myocytes (NRVCs). miR-98 overexpression remarkably increased cell viability and inhibited apoptosis of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated NRVCs. Meanwhile, overexpression of miR-98 reversed H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-induced Bcl-2 downregulation and Bax elevation and significantly reduced JC-1 monomeric cells. Meanwhile, miR-98 overexpression attenuated the upregulation of Fas and caspase-3 in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-treated cardiomyocytes at the mRNA and protein levels. Dual-luciferase reporter assay showed that miR-98 directly targeted to Fas 3\u2032-UTR. Furthermore, MI mice injected with miR-98-agomir had a significant reduction of apoptotic cells, the serum LDH levels, myocardial caspase-3 activity, Fas and caspase-3 expression in heart tissues. Administration of miR-98-agomir also showed decreased infarct size and improved cardiac function. Collectively, miR-98 is downregulated in the MI heart and NRVCs in response to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> stress, and miR-98 overexpression protects cardiomyocytes against apoptosis. Anti-apoptotic effects of miR-98 are associated with regulation of Fas\/Caspase-3 apoptotic signal pathway.<\/jats:p>","DOI":"10.1038\/s41598-017-07578-x","type":"journal-article","created":{"date-parts":[[2017,8,1]],"date-time":"2017-08-01T15:05:39Z","timestamp":1501599939000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["MicroRNA-98 negatively regulates myocardial infarction-induced apoptosis by down-regulating Fas and caspase-3"],"prefix":"10.1038","volume":"7","author":[{"given":"Chuan","family":"Sun","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huibin","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Di","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"He","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhimin","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,8,7]]},"reference":[{"key":"7578_CR1","doi-asserted-by":"publisher","first-page":"e85","DOI":"10.1161\/CIRCULATIONAHA.105.171600","volume":"113","author":"T Thom","year":"2006","unstructured":"Thom, T. et al. 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