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However, the functions of mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> in hepatitis C virus (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>)\u2010related liver fibrosis remain unclear. In this study, we systematically analyzed the microarray data of the serum mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> in patients with <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010induced hepatic fibrosis. Among 41 dysregulated mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>, miR\u20101273g\u20103p was the most significantly upregulated mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and correlated with the stage of liver fibrosis. Overexpression of miR\u20101273g\u20103p could inhibit translation of <jats:styled-content style=\"fixed-case\">PTEN<\/jats:styled-content>, increase the expression of \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>, Col1A1, and reduce apoptosis in <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content>s. Hence, we conclude that miR\u20101273g\u20103p might affect the activation and apoptosis of <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content>s by directly targeting <jats:styled-content style=\"fixed-case\">PTEN<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010related liver fibrosis<jats:bold>.<\/jats:bold><\/jats:p>","DOI":"10.1002\/1873-3468.12309","type":"journal-article","created":{"date-parts":[[2016,7,16]],"date-time":"2016-07-16T14:26:43Z","timestamp":1468679203000},"page":"2709-2724","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["miR\u20101273g\u20103p modulates activation and apoptosis of hepatic stellate cells by directly targeting <scp>PTEN<\/scp> in <scp>HCV<\/scp>\u2010related liver fibrosis"],"prefix":"10.1002","volume":"590","author":[{"given":"Xuemin","family":"Niu","sequence":"first","affiliation":[{"name":"Department of 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