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Liver\u2010specific IGF\u20101\u2010deficient (LID) and C57\/BL6 mice were subject to AAC. Echocardiographic and cardiomyocyte function were assessed 4 wks later. Haematoxylin and eosin staining was used to monitor myocardial morphology. Western blot and real\u2010time PCR were used to detect protein and miR expression, respectively. Neonatal rat cardiomyocytes (NRCMs) were transfected with miRs prior to IGF\u20101 exposure to initiate cell proliferation. Immunohistochemistry and [<jats:sup>3<\/jats:sup>H] Leucine incorporation were used to detect cell surface area and protein abundance. C57 mice subject to AAC displayed increased ventricular wall thickness, decreased left ventricular end diastolic and end systolic dimensions and elevated cardiomyocyte shortening capacity, all of which were attenuated in LID mice. In addition, IGF\u20101 deficiency mitigated AAC\u2010induced increase in atrial natriuretic factor, GATA binding protein 4, glucose transporter 4 (GLUT4) and Akt phosphorylation. In contrast, neither AAC treatment nor IGF\u20101 deficiency affected glycogen synthase kinase 3b, mammalian target of rapamycin, the Glut\u20104 translocation mediator Akt substrate of 160 kD (AS160) and protein phosphatase. Levels of miR\u20101 and \u2010133a (but not miR\u2010208) were significantly attenuated by AAC in C57 but not LID mice. Transfection of miR\u20101 and \u2010133a obliterated IGF\u20101\u2010induced hypertrophic responses in NRCMs. Our data suggest that IGF\u20101 deficiency retards AAC\u2010induced cardiac hypertrophic and contractile changes\u2002<jats:italic>via<\/jats:italic>\u2002alleviating down\u2010regulation of miR\u20101 and miR\u2010133a in response to left ventricular pressure overload.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2011.01307.x","type":"journal-article","created":{"date-parts":[[2011,3,21]],"date-time":"2011-03-21T19:23:05Z","timestamp":1300735385000},"page":"83-95","source":"Crossref","is-referenced-by-count":88,"title":["IGF\u20101 deficiency resists cardiac hypertrophy and myocardial contractile dysfunction: role of microRNA\u20101 and 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