{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:24:43Z","timestamp":1791296683965,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,1,11]],"date-time":"2012-01-11T00:00:00Z","timestamp":1326240000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiac hypertrophy, which is characterized by the enlargement of cell size, reactivation of fetal genes, remains one of the most important triggers to heart failure. Increasing evidence shows that microRNA (miRNA) is extensively involved in the pathogenesis of cardiac hypertrophy. But the effects of miRNAs on cardiomyocyte hypertrophy have not been completely solved yet. Here, we showed that a collection of miRNAs was aberrantly expressed in hypertrophic cardiomyocytes induced by phenylephrine (PE) or angiotensin II (Ang II). Among them, miR\u201022 was the most strikingly up\u2010regulated miRNA. To investigate the role of miR\u201022 in hypertrophy, both over\u2010expression and knock\u2010down assays were performed on cardiomyocytes. The results showed that up\u2010regulation of miR\u201022 significantly increased the cell size and markedly influenced the expression of hypertrophic markers, including induction of <jats:italic>nppa<\/jats:italic> and reduction of <jats:italic>myh6<\/jats:italic>. In contrast, reduction of miR\u201022 level attenuated either PE\u2010 or Ang II\u2010induced hypertrophic reaction. Furthermore, several genes, including PTEN, were identified as potential targets of miR\u201022 by bioinformatic algorithms. Using luciferase analysis, miR\u201022 could significantly suppress the luciferase activity of reporter fused with 3\u2032 untranslated region of PTEN mRNA. Furthermore, up\u2010regulation of miR\u201022 could suppress the protein level of PTEN and reduction of miR\u201022 level markedly increased the protein level of PTEN in cardiomyocytes by Western blot analysis, suggesting that the contribution of miR\u201022 to cardiomyocyte hypertrophy may be partially through targeting PTEN. Taken together, miRNAs were dynamically regulated in cardiomyocyte hypertrophy and attenuation of miR\u201022 in rat cardiomyocytes efficiently protected from hypertrophic effects through derepressing PTEN. J. Cell. Physiol. 227: 1391\u20131398, 2012. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22852","type":"journal-article","created":{"date-parts":[[2011,5,26]],"date-time":"2011-05-26T13:00:24Z","timestamp":1306414824000},"page":"1391-1398","source":"Crossref","is-referenced-by-count":89,"title":["Attenuation of MicroRNA\u201022 derepressed PTEN to effectively protect rat cardiomyocytes from 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