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Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy
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SYSNO ASEP 0550595 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy Author(s) Fernandez, C. (CL)
Torrealba, Natalia (BTO-N)
Altamirano, F. (US)
Garrido-Moreno, V. (CL)
Vasquez-Trincado, C. (CL)
Flores-Vergara, R. (CL)
Lopez-Crisosto, C. (CL)
Ocaranza, M. P. (CL)
Chiong, M. (CL)
Pedrozo, Z. (CL)
Lavandero, S. (CL)Number of authors 11 Article number e0255452 Source Title PLoS ONE. - : Public Library of Science - ISSN 1932-6203
Roč. 16, č. 8 (2021)Number of pages 15 s. Language eng - English Country US - United States Keywords factor-i receptor ; cardiac-hypertrophy ; protein ; calcium ; deletion Subject RIV EB - Genetics ; Molecular Biology OECD category Biochemistry and molecular biology Method of publishing Open access Institutional support BTO-N - RVO:86652036 UT WOS 000686033500008 DOI 10.1371/journal.pone.0255452 Annotation 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. Workplace Institute of Biotechnology Contact Monika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700 Year of Publishing 2022 Electronic address https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0255452
Number of the records: 1