Neuropeptide Y induces cardiomyocyte hypertrophy via calcineurin signaling in rats

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• 作者：Chen ; Minsheng ; Li ; Xiaoyun ; Dong ; Qi ; Li ; Yinghui ; Liang ; Wenbin
• 关键词：Neuropeptide Y ; Calcineurin ; Cardiac hypertrophy ; Ca²⁺ signaling
• 刊名：Regulatory Peptides
• 出版年：2005
• 期刊代码：68_01670115
• 类别：neu
• 出版时间：February 15, 2005
• 卷：125
• 期：1-3
• 页码：9-15
• 文件大小：459 K

摘要

Neuropeptide Y (NPY) has been shown to participate in cardiac hypertrophy. However, the mechanisms by which NPY induces cardiomyocyte hypertrophy are poorly understood. This study tested the hypothesis that NPY induces cardiomyocyte hypertrophy through Ca²⁺/CaM-dependent calcineurin (CaN) pathway in cultured neonatal rat cardiomyocytes. After 24-h treatment, NPY (100 nM) significantly increased ³H-leucine incorporation and c-Jun mRNA expression, concomitant with augment of CaN activity and protein level in cardiomyocytes compared to those cells without NPY treatment. The enhancement of ³H-leucine incorporation and c-Jun mRNA expression in cardiomyocytes treated with NPY were markedly inhibited by cyclosporine A (CsA), a selective inhibitor of CaN. We also investigated the effect of NPY on intracellular Ca²⁺ level in cardiomyocytes. There were no obvious changes in intracellular Ca²⁺ level of cytoplasm and nucleus in cardiomyocytes treated with NPY (100 nM) for 10 min. However, NPY significantly increased intracellular Ca²⁺ level of cytoplasm and nucleus in cardiomyocytes after 24-h treatment. The result suggested that NPY could induce hypertrophy of cardiomyocytes via Ca²⁺/CaM-dependent CaN signal pathway. The enhancement of [Ca²⁺]_i caused by NPY may activate CaN signal pathways to mediate cardiac hypertrophy.