Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy

Carolina Fernández, Natalia Torrealba, Francisco Altamirano, Valeria Garrido- Moreno, César Vásquez-Trincado, Raúl Flores-Vergara, Camila López-Crisosto, María Paz Ocaranza, Mario Chiong, Zully Pedrozo, Sergio Lavandero

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4 Scopus citations


Cardiac hypertrophy is the result of responses to various physiological or pathological stimuli. Recently, we showed that polycystin-1 participates in cardiomyocyte hypertrophy elicited by pressure overload and mechanical stress. Interestingly, polycystin-1 knockdown does not affect phenylephrine-induced cardiomyocyte hypertrophy, suggesting that the effects of polycystin-1 are stimulus-dependent. In this study, we aimed to identify the role of polycystin-1 in insulin-like growth factor-1 (IGF-1) signaling in cardiomyocytes. Polycystin-1 knockdown completely blunted IGF-1-induced cardiomyocyte hypertrophy. We then investigated the molecular mechanism underlying this result. We found that polycystin-1 silencing impaired the activation of the IGF-1 receptor, Akt, and ERK1/2 elicited by IGF-1. Remarkably, IGF-1-induced IGF-1 receptor, Akt, and ERK1/2 phosphorylations were restored when protein tyrosine phosphatase 1B was inhibited, suggesting that polycystin-1 knockdown deregulates this phosphatase in cardiomyocytes. Moreover, protein tyrosine phosphatase 1B inhibition also restored IGF-1-dependent cardiomyocyte hypertrophy in polycystin-1- deficient cells. Our findings provide the first evidence that polycystin-1 regulates IGF-1- induced cardiomyocyte hypertrophy through a mechanism involving protein tyrosine phosphatase 1B.

Original languageEnglish (US)
Article numbere0255452
JournalPLoS ONE
Issue number8 August
StatePublished - Aug 2021

ASJC Scopus subject areas

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