Key result
miR-145 protected against isoproterenol-induced cardiomyocyte hypertrophy by targeting the expression and localization of GATA6.
miR-145 acts as a protective regulator against pathological cardiac hypertrophy by targeting GATA6, highlighting its potential as a therapeutic target for heart failure.
Should not alter clinical practice; extends preclinical evidence for miR-145 in hypertrophy models.
Excessive βAR stimulation is an independent factor in inducing pathological cardiac hypertrophy. Here, we report miR-145 regulates both expression and localization of GATA6, thereby protecting the heart against cardiomyocyte hypertrophy induced by isoproterenol (ISO). The protective activity of miR-145 was associated with down-regulation of ANF, BNP and β-MHC expression, a decreased rate of protein synthesis, inhibited cardiomyocyte growth and the modulation of several signaling pathways including ERK1/2, JNK and Akt-GSK3β. The anti-hypertrophic effect was abrogated by exogenous over-expression of transcription factor GATA6 which was further identified as a direct target of miR-145. In addition, GSK3β antagonists, LiCl and TDZD8, restored the nuclear accumulation of GATA6, which was attenuated by miR-145 Finally, we observed a dynamic pattern of miR-145 expression in ISO-treated NRCMs and in the hearts of TAC mice. Together, our results identify miR-145 as an important regulator in cardiac hypertrophy.
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Li et al. (2013) studied Cardiac hypertrophy. miR-145 was evaluated on Cardiomyocyte hypertrophy. miR-145 protected against isoproterenol-induced cardiomyocyte hypertrophy by targeting the expression and localization of GATA6.
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