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- W1497668882 abstract "Obesity is associated with increased leptin production which may contribute to cardiac hypertrophy. However, the mechanism of leptin-induced cardiac hypertrophy remains incompletely understood. The Rho family and mTOR have recently emerged as important regulators of cell growth. In this study we explored the roles of phosphatidylinositol 3-kinase (PI3K), mTOR and the Rho family in the regulation of actin polymerization in leptin-induced hypertrophy in cultured neonatal rat cardiomyocytes treated with 3.1 nM leptin. Leptin treatment resulted in activation of RhoA and Rac1 (by 330% and 160%, respectively; P<0.05) but not cdc42, 5 min after treatment, as determined by Western blotting. The hypertrophic effect of leptin was associated with an increase in phosphorylation of p70S6K by 110% (P<0.05). The specific mTOR inhibitor, rapamycin (10 nM) attenuated leptin-induced RhoA and Rac1 activation. Furthermore, the decrease in the G/F actin ratio, a measure of actin polymerization, was blunted by rapamycin. Leptin produced activation of the transcriptional factor GATA-4 which was attenuated by the RhoA inhibitor C3, the p38 MAPK inhibitor SB203580 (10 µM) or rapamycin. Our results demonstrate that leptin-induced cardiomyocyte hypertrophy is associated with GATA-4 activation which is dependent on RhoA, PI3K/mTOR/p70S6K and p38 MAPK pathways. Supported by the Canadian Institutes of Health Research." @default.
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- W1497668882 date "2009-04-01" @default.
- W1497668882 modified "2023-09-27" @default.
- W1497668882 title "RhoA links PI3K/Akt/mTOR signaling to p38 MAPK/GATA‐4 activation in leptin–induced cardiomyocyte hypertrophy" @default.
- W1497668882 doi "https://doi.org/10.1096/fasebj.23.1_supplement.577.7" @default.
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