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1 Internal Medicine II, University of Yamanashi, Faculty of Medicine, Yamanashi-prefecture, Japan
* To whom correspondence should be addressed. E-mail: kugiyama{at}yamanashi.ac.jp.
Adiponectin, an adipocyte-derived protein, has cardioprotective actions. We elucidated the role of adiponectin receptors, AdipoR1 and AdipoR2, in the effects of adiponectin on endothelin (ET)-1-induced hypertrophy in cultured cardiomyocytes and we also examined the expression of adiponectin receptors in normal and infarcted mice hearts. This study showed that recombinant full-length adiponectin suppressed the ET-1-induced increase in cell surface area and [3H] leucine incorporation into cultured cardiomyocytes, compared to the cells treated with ET-1 alone. Transfection of siRNA specific for AdipoR1 or AdipoR2 reversed the suppressive effects of adiponectin on ET-1-induced cell hypertrophy in cultured cardiomyocytes. Adiponectin induced phosphorylation of AMP-activated protein kinase (AMPK) and inhibited ET-1-induced ERK1/2 phosphorylation, which were also reversible by transfection of siRNA for AdipoR1 or AdipoR2 in cultured cardiomyocytes. Transfection of siRNA for 
2 catalytic subunits of AMPK reduced the inhibitory effects of adiponectin on ET-1-induced cell hypertrophy and ERK1/2 phosphorylation. Globular adiponectin showed similar effects as full-length adiponectin, and siRNA for AdipoR1 reversed the actions of globular adiponectin. Compared to normal left ventricle, expression levels of AdipoR1 mRNA and protein were decreased in the remote area as well as the infarcted area after myocardial infarction in mice hearts. In conclusion, AdipoR1 and AdipoR2 mediate the suppressive effects of full-length and globular adiponectin on ET-1-induced hypertrophy in the cultured cardiomyocytes, and AMPK is involved in signal transduction through these receptors. The adiponectin receptors, AdipoR1 and AdipoR2, might play a role in the pathogenesis of ET-1-related cardiomyocytes hypertrophy after myocardial infarction.
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