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Micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s are recognised as important epigenetic regulators of endothelial function. The aim of this study was to determine the roles of micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s in angiogenesis. Eighteen circulating micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s including miR\u2010185\u20105p were differently expressed in plasma from patients with <jats:styled-content style=\"fixed-case\">ACS<\/jats:styled-content> by high\u2010throughput <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> sequencing. The expressional levels of miR\u2010185\u20105p were dramatically reduced in hearts isolated from mice following <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> and cultured human umbilical vein endothelial cells (<jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s) under hypoxia, as determined by fluorescence in\u00a0situ hybridisation and quantitative <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>. Evidence from computational prediction and luciferase reporter gene activity indicated that cathepsin K (CatK) <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> is a target of miR\u2010185\u20105p. In <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s, miR\u2010185\u20105p mimics inhibited cell proliferations, migrations and tube formations under hypoxia, while miR\u2010185\u20105p inhibitors performed the opposites. Further, the inhibitory effects of miR\u2010185\u20105p up\u2010regulation on cellular functions of <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s were abolished by CatK gene overexpression, and adenovirus\u2010mediated CatK gene silencing ablated these enhancive effects in <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>s under hypoxia. In vivo studies indicated that gain\u2010function of miR\u2010185\u20105p by agomir infusion down\u2010regulated CatK gene expression, impaired angiogenesis and delayed the recovery of cardiac functions in mice following <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. These actions of miR\u2010185\u20105p agonists were mirrored by in\u00a0vivo knockdown of CatK in mice with <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. Endogenous reductions of miR\u2010185\u20105p in endothelial cells induced by hypoxia increase CatK gene expression to promote angiogenesis and to accelerate the recovery of cardiac function in mice following <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/jcmm.14016","type":"journal-article","created":{"date-parts":[[2018,11,19]],"date-time":"2018-11-19T02:35:09Z","timestamp":1542594909000},"page":"1164-1173","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Endogenous reduction of miR\u2010185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K"],"prefix":"10.1111","volume":"23","author":[{"given":"Chuan\u2010Chang","family":"Li","sequence":"first","affiliation":[{"name":"Department of Geriatric Medicine Xiangya Hospital Central South University Changsha China"},{"name":"National Clinical Research Center for 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