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Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy
- 1.0550595 - BTÚ 2022 RIV US eng J - Článek v odborném periodiku
Fernandez, C. - Torrealba, Natalia - Altamirano, F. - Garrido-Moreno, V. - Vasquez-Trincado, C. - Flores-Vergara, R. - Lopez-Crisosto, C. - Ocaranza, M. P. - Chiong, M. - Pedrozo, Z. - Lavandero, S.
Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
PLoS ONE. Roč. 16, č. 8 (2021), č. článku e0255452. ISSN 1932-6203. E-ISSN 1932-6203
Institucionální podpora: RVO:86652036
Klíčová slova: factor-i receptor * cardiac-hypertrophy * protein * calcium * deletion
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 3.752, rok: 2021
Způsob publikování: Open access
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.
Trvalý link: http://hdl.handle.net/11104/0327370
Počet záznamů: 1