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

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dc.catalogadordfo
dc.contributor.authorFernández, Carolina
dc.contributor.authorTorrealba, Natalia
dc.contributor.authorAltamirano, Francisco
dc.contributor.authorGarrido-Moreno, Valeria
dc.contributor.authorVásquez-Trincado, César
dc.contributor.authorFlores-Vergara, Raúl
dc.contributor.authorLópez-Crisosto, Camila
dc.contributor.authorOcaranza Jeraldino, María Paz
dc.contributor.authorChiong, Mario
dc.contributor.authorZ, Pedrozo
dc.contributor.authorLavandero, Sergio
dc.date.accessioned2024-06-06T16:32:04Z
dc.date.available2024-06-06T16:32:04Z
dc.date.issued2021
dc.description.abstractCardiac 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.
dc.fechaingreso.objetodigital2024-06-06
dc.fuente.origenORCID
dc.identifier.doi10.1371/journal.pone.0255452
dc.identifier.urihttp://dx.doi.org/10.1371/journal.pone.0255452
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/86549
dc.information.autorucEscuela de Medicina; Ocaranza Jeraldino, Maria Paz; 0000-0002-4915-6378; 1001254
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final15
dc.pagina.inicio1
dc.revistaPLoS One
dc.rightsacceso abierto
dc.rights.licenseAttribution 4.0 International (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titlePolycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy
dc.typeartículo
sipa.codpersvinculados1001254
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