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

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    SYSNO ASEP0550595
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevPolycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy
    Tvůrce(i) 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)
    Celkový počet autorů11
    Číslo článkue0255452
    Zdroj.dok.PLoS ONE - ISSN 1932-6203
    Roč. 16, č. 8 (2021)
    Poč.str.15 s.
    Jazyk dok.eng - angličtina
    Země vyd.US - Spojené státy americké
    Klíč. slovafactor-i receptor ; cardiac-hypertrophy ; protein ; calcium ; deletion
    Vědní obor RIVEB - Genetika a molekulární biologie
    Obor OECDBiochemistry and molecular biology
    Způsob publikováníOpen access
    Institucionální podporaBTO-N - RVO:86652036
    UT WOS000686033500008
    DOI10.1371/journal.pone.0255452
    AnotaceCardiac 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.
    PracovištěBiotechnologický ústav
    KontaktMonika Kopřivová, Monika.Koprivova@ibt.cas.cz, Tel.: 325 873 700
    Rok sběru2022
    Elektronická adresahttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0255452
Počet záznamů: 1