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SCIMIA, Maria Cecilia; HURTADO, Cecilia; BUENO, Orlando F; VLASUK, George P; KALIMAN, Perla; BODMER, Rolf; SMITH, Layton H; ASHLEY, Euan; MERCOLA, Mark; BROWN, Joan Heller; RUIZ-LOZANO, Pilar; RAY, Saugata; METZLER, Scott; KE WEI; JIANMING WANG; WOODS, Chris E; PURCELL, NicoleH; CATALUCCI, Daniele; AKASAKA, Takeshi
Nature (London), 08/2012, Letnik: 488, Številka: 7411Journal Article
Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypertrophy and heart failure. In contrast, mice lacking apelin (the endogenous APJ ligand) remain sensitive, suggesting an apelin-independent function of APJ. Freshly isolated APJ-null cardiomyocytes exhibit an attenuated response to stretch, indicating that APJ is a mechanosensor. Activation of APJ by stretch increases cardiomyocyte cell size and induces molecular markers of hypertrophy. Whereas apelin stimulates APJ to activate Gαi and elicits a protective response, stretch signals in an APJ-dependent, G-protein-independent fashion to induce hypertrophy. Stretch-mediated hypertrophy is prevented by knockdown of β-arrestins or by pharmacological doses of apelin acting through Gαi. Taken together, our data indicate that APJ is a bifunctional receptor for both mechanical stretch and the endogenous peptide apelin. By sensing the balance between these stimuli, APJ occupies a pivotal point linking sustained overload to cardiomyocyte hypertrophy.
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