Essential role of TRPC1 channels in cardiomyoblasts hypertrophy mediated by 5-HT2A serotonin receptors

被引：34
|
作者：
Vindis, Cecile [1 ]
D'Angelo, Romina [2 ]
Mucher, Elodie [1 ]
Negre-Salvayre, Anne [1 ]
Parini, Angelo [3 ]
Mialet-Perez, Jeanne [3 ]
机构：
[1] CHU Rangueil, INSERM, U 858 12MR, IFR 150,Dept Vasc Biol, F-31054 Toulouse, France
[2] CHU Rangueil, INSERM, U 858 12MR,Cellular Imaging Facil, IFR 150 TRI Plateform, F-31054 Toulouse, France
[3] CHU Rangueil, INSERM, U 858 12MR, IFR 150,Dept Cardiac Remodeling, F-31054 Toulouse, France
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2010年 / 391卷 / 01期
关键词：
5-HT2A receptors; 5-HT; TRPC; NFAT; Cardiac hypertrophy; CARDIOMYOCYTE HYPERTROPHY; VENTRICULAR HYPERTROPHY; POTENTIAL CHANNELS; ANGIOTENSIN-II; ACTIVATION;
D O I：
10.1016/j.bbrc.2009.12.001
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Serotonin (5-HT) paiticipates in the development of cardiac hypertrophy through 5-HT2A serotonin receptors. The hypertrophic growth of cardiomyoblasts induced by 5-HT2A receptors involves the activation of the Ca2+ responsive calcineurin/NFAT pathway However, the mechanism whereby NFAT is activated by 5-HT2A receptors remains indeterminate In this study, we examined whether transient receptor potential canonical (TRPC) channels participate in NFAT activation and hypertrophic response triggered by 5-HT We demonstrate that TRPC1 expression is upregulated in 5-HT-treated rat cardiomyoblasts whereas TRPC6 is induced in a mouse Model of heart hypertrophy Moreover, TRPC1 knockdown by small interfering RNA inhibits NFAT activation and hypertrophic response mediated by 5-HT2A receptors These findings provide new insights about a mechanistic basis for the activation of the calcineurin/NFAT pathway by 5-HT2A receptors and highlight the critical role of TRPC1 in the development of cardiac hypertrophy. (C) 2009 Elsevier Inc. All rights reserved
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收藏
页码：979 / 983
页数：5
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