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TRPC1 通道在 5-HT2A 血清素受体介导的心肌细胞肥大中的重要作用。

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

机构信息

Department of Vascular Biology, IFR150, CHU Rangueil, INSERM U-858/I2MR, Toulouse, France.

出版信息

Biochem Biophys Res Commun. 2010 Jan 1;391(1):979-83. doi: 10.1016/j.bbrc.2009.12.001. Epub 2009 Dec 11.

DOI:10.1016/j.bbrc.2009.12.001
PMID:20005206
Abstract

Serotonin (5-HT) participates in the development of cardiac hypertrophy through 5-HT(2A) serotonin receptors. The hypertrophic growth of cardiomyoblasts induced by 5-HT(2A) receptors involves the activation of the Ca(2+) responsive calcineurin/NFAT pathway. However, the mechanism whereby NFAT is activated by 5-HT(2A) 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-HT(2A) receptors. These findings provide new insights about a mechanistic basis for the activation of the calcineurin/NFAT pathway by 5-HT(2A) receptors and highlight the critical role of TRPC1 in the development of cardiac hypertrophy.

摘要

血清素（5-HT）通过 5-HT（2A）血清素受体参与心肌肥厚的发展。5-HT（2A）受体诱导的心肌细胞肥大涉及钙响应型钙调神经磷酸酶/NFAT 通路的激活。然而，5-HT（2A）受体激活 NFAT 的机制尚不确定。在这项研究中，我们研究了瞬时受体电位经典（TRPC）通道是否参与 5-HT 触发的 NFAT 激活和心肌肥厚反应。我们证明，5-HT 处理的大鼠心肌细胞中 TRPC1 表达上调，而心脏肥厚的小鼠模型中 TRPC6 被诱导。此外，小干扰 RNA 敲低 TRPC1 抑制 5-HT（2A）受体介导的 NFAT 激活和心肌肥厚反应。这些发现为 5-HT（2A）受体激活钙调神经磷酸酶/NFAT 通路的机制基础提供了新的见解，并强调了 TRPC1 在心脏肥厚发展中的关键作用。

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