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Mild hypoxia (MH, 10% O<jats:sub>2<\/jats:sub>) caused hypertrophy in cultured neonatal rat cardiac myocytes, which was accompanied with increase of HIF\u20101\u03b1 mRNA and accumulation of HIF\u20101\u03b1 protein in nuclei. Transient receptor potential canonical (TRPC) channels including TRPC3 and TRPC6, except for TRPC1, were increased, and Ca<jats:sup>2+<\/jats:sup>\u2010calcineurin signals were also enhanced in a time\u2010dependent manner under MH condition. MH\u2010induced cardiomyocytes hypertrophy, TRPC up\u2010regulation and enhanced Ca<jats:sup>2+<\/jats:sup>\u2010calcineurin signals were inhibited by an HIF\u20101\u03b1 specific blocker, SC205346 (30 \u03bcM), whereas promoted by HIF\u20101\u03b1 overexpression. Electrophysiological voltage\u2010clamp demonstrated that DAG analogue, OAG (30 \u03bcM), induced TRPC current by as much as 170% in neonatal rat cardiomyocytes overexpressing HIF\u20101\u03b1 compared to negative control. These results implicate that HIF\u20101\u03b1 plays a key role in development of cardiac hypertrophy in responses to hypoxic stress. Its mechanism is associated with up\u2010regulating TRPC3, TRPC6 expression, activating TRPC current and subsequently leading to enhanced Ca<jats:sup>2+<\/jats:sup>\u2010calcineurin signals.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2011.01497.x","type":"journal-article","created":{"date-parts":[[2011,12,1]],"date-time":"2011-12-01T16:24:00Z","timestamp":1322756640000},"page":"2022-2034","source":"Crossref","is-referenced-by-count":45,"title":["Mild hypoxia\u2010induced cardiomyocyte hypertrophy <i>via<\/i> up\u2010regulation of HIF\u20101\u03b1\u2010mediated TRPC 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