Glycine prevents pressure overload induced cardiac hypertrophy mediated by glycine receptor
Glycine prevents pressure overload induced cardiac hypertrophy mediated by glycine receptor
复制标题
甘氨酸可防止甘氨酸受体介导的压力超负荷引起的心脏肥大
DOI：
10.1016/j.bcp.2016.11.008
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发表时间：
2017-01-01
影响因子：
5.8
通讯作者：
Chen, Qi
中科院分区：
文献类型：
--
作者：
Lu, Yan;Zhu, Xudong;Chen, Qi
作为一种主要的氨基酸，甘氨酸在代谢、生长、免疫、细胞保护和存活中具有多种功能。本研究的目的是确定甘氨酸对病理性心肌肥厚的影响及其机制。甘氨酸预处理显著减弱由横主动脉缩窄或血管紧张素II（Ang II）引起的小鼠心肌肥厚。这种作用与心肌细胞外信号调节激酶1/2磷酸化的抑制有关。当内源性甘氨酸受体α 2通过mRNA干扰被敲低时，甘氨酸的心脏保护作用消失。共培养实验表明，甘氨酸也可以拮抗血管紧张素II刺激释放的转化生长因子β和内皮素-1的心肌细胞，防止过度生产的胶原在大鼠成纤维细胞。这些结果，首次表明，甘氨酸可能是一种新的心脏保护剂对压力超负荷诱导的心肌肥大。因此，甘氨酸可用于预防心脏肥大和心力衰竭。(c)2016 Elsevier Inc. All rights reserved.
As a major amino acid, glycine has multiple functions in metabolism, growth, immunity, cytoprotection, and survival. The aim of this study was to determine the effects of glycine on pathologic cardiac hypertrophy and the mechanism underlying it. Pre-treatment with glycine significantly attenuated murine cardiac hypertrophy induced by transverse aortic constriction or by administration of angiotensin II (Ang II). This action was associated with a suppressive extracellular signal-regulated kinase 1/2 phosphorylation in myocardium. The cardioprotective effect of glycine disappeared when endogenous glycine receptor alpha 2 was knocked down by mRNA interference in rats. Co-culture experiments revealed that glycine could also antagonize Ang II stimulated release of transforming growth factor beta and endothelin-1 by cardiomyocytes, which prevented an over-production of collagens in rat fibroblasts. These results, for the first time, demonstrate that glycine may be a novel cardioprotector against pressure overload induced cardiac hypertrophy. Thus, glycine would be useful in the prevention of cardiac hypertrophy and heart failure. (c) 2016 Elsevier Inc. All rights reserved.