{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T03:50:08Z","timestamp":1789617008498,"version":"build-2803163510"},"reference-count":27,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2012,10,29]],"date-time":"2012-10-29T00:00:00Z","timestamp":1351468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2012,11]]},"abstract":"Abstract<\/jats:title>MicroRNA<\/jats:styled-content>s (miRNA<\/jats:styled-content>s) are small, regulatory non\u2010coding RNA<\/jats:styled-content>s that have potent effects on gene expression. Several miRNA<\/jats:styled-content> are deregulated in cellular processes involved in human liver diseases and regulation of cellular processes. Recent studies have identified the involvement of miR<\/jats:styled-content>\u201029 in hepatic fibrosis and carcinogenesis. Although several targets of miR<\/jats:styled-content>\u201029 have been identified, there is limited information regarding the cell\u2010type specific roles of miR<\/jats:styled-content>\u201029 in the liver, and we sought to evaluate the role of this miRNA<\/jats:styled-content> in hepatic pathobiology. We report the generation of a tissue\u2013specific knockout mouse to evaluate the role of miR<\/jats:styled-content>\u201029 in hepatic fibrosis and carcinogenesis in response to injury. We hypothesized that miR<\/jats:styled-content>\u201029 contributes to the hepatocyte driven response to chronic cellular injury that results in fibrosis. In support of this hypothesis, fibrosis and mortality were enhanced in miR<\/jats:styled-content>29 knockout mice in response to carbon tetrachloride. Genome\u2010wide gene expression analysis identified an over\u2010representation of genes associated with fibrosis. The oncofetal RNA H<\/jats:styled-content>19 was modulated in a miR<\/jats:styled-content>\u201029 dependent manner following exposure to carbon tetrachloride in vivo<\/jats:italic>. The impact of a hepatocyte specific miR<\/jats:styled-content>\u201029 knockout on survival following chronic hepatic injury in vivo<\/jats:italic> implicates this miRNA<\/jats:styled-content> as a potential target for intervention. These results provide evidence of the involvement of miR<\/jats:styled-content>\u201029 in chronic hepatic injury, and suggest a role for deregulated hepatocyte expression of miR<\/jats:styled-content>\u201029 in the response to hepatic injury, fibrosis and carcinogenesis.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2012.01578.x","type":"journal-article","created":{"date-parts":[[2012,4,3]],"date-time":"2012-04-03T17:00:50Z","timestamp":1333472450000},"page":"2647-2654","source":"Crossref","is-referenced-by-count":51,"title":["Hepatic miR<\/scp>\u201029ab1 expression modulates chronic hepatic injury"],"prefix":"10.1111","volume":"16","author":[{"given":"Takayuki","family":"Kogure","sequence":"first","affiliation":[{"name":"College of Medicine Ohio State University Columbus OH USA"},{"name":"Department of Transplantation, Division of Gastroenterology and Hepatology Mayo Clinic Jacksonville FL 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