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

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-in...

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Autores principales:	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
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/282852eddbe64e25877af76197d62e17
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spelling	oai:doaj.org-article:282852eddbe64e25877af76197d62e172021-12-02T20:17:52ZPolycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.1932-620310.1371/journal.pone.0255452https://doaj.org/article/282852eddbe64e25877af76197d62e172021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0255452https://doaj.org/toc/1932-6203Cardiac 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.Carolina FernándezNatalia TorrealbaFrancisco AltamiranoValeria Garrido-MorenoCésar Vásquez-TrincadoRaúl Flores-VergaraCamila López-CrisostoMaría Paz OcaranzaMario ChiongZully PedrozoSergio LavanderoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 8, p e0255452 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q 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 Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
description	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.
format	article
author	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
author_facet	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
author_sort	Carolina Fernández
title	Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
title_short	Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
title_full	Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
title_fullStr	Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
title_full_unstemmed	Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
title_sort	polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/282852eddbe64e25877af76197d62e17
work_keys_str_mv	AT carolinafernandez polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT nataliatorrealba polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT franciscoaltamirano polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT valeriagarridomoreno polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT cesarvasqueztrincado polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT raulfloresvergara polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT camilalopezcrisosto polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT mariapazocaranza polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT mariochiong polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT zullypedrozo polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy AT sergiolavandero polycystin1isrequiredforinsulinlikegrowthfactor1inducedcardiomyocytehypertrophy
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Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy.

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