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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload
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Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload

机译：G蛋白信号调节剂5在压力超负荷的生物力学应力作用下可防止心脏肥大和纤维化

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摘要

The development of cardiac hypertrophy in response to increased hemodynamic load and neurohormonal stress is initially a compensatory response that may eventually lead to ventricular dilation and heart failure. Regulator of G protein signaling 5 (Rgs5) is a negative regulator of G protein-mediated signaling by inactivating Gα(q) and Gα(i), which mediate actions of most known vasoconstrictors. Previous studies have demonstrated that Rgs5 expresses among various cell types within mature heart and showed high levels of Rgs5 mRNA in monkey and human heart tissue by Northern blot analysis. However, the critical role of Rgs5 on cardiac remodeling remains unclear. To specifically determine the role of Rgs5 in pathological cardiac remodeling, we used trans-genic mice with cardiac-specific overexpression of human Rgs5 gene and Rgs5~(-/-) mice. Our results demonstrated that the trans-genic mice were resistant to cardiac hypertrophy and fibrosis through inhibition of MEK-ERK1/2 signaling, whereas the Rgs5~(-/-) mice displayed the opposite phenotype in response to pressure overload. These studies indicate that Rgs5 protein is a crucial component of the signaling pathway involved in cardiac remodeling and heart failure.
机译：响应于增加的血流动力学负荷和神经激素压力而发生的心肌肥大最初是一种代偿性反应，最终可能导致心室扩张和心力衰竭。 G蛋白信号传导调节剂5（Rgs5）是通过失活Gα（q）和Gα（i）来介导大多数已知血管收缩剂作用的G蛋白介导信号传导的负调节剂。先前的研究表明，Rgs5在成熟心脏内的各种细胞类型中表达，并通过Northern印迹分析显示在猴和人心脏组织中Rgs5 mRNA高水平。然而，Rgs5在心脏重塑中的关键作用仍不清楚。为了具体确定Rgs5在病理性心脏重塑中的作用，我们使用了具有人特异性Rgs5基因过度表达的转基因小鼠和Rgs5〜（-/-）小鼠。我们的结果表明，转基因小鼠通过抑制MEK-ERK1 / 2信号转导对心肌肥大和纤维化具有抗性，而Rgs5〜（-/-）小鼠在压力超负荷时表现出相反的表型。这些研究表明，Rgs5蛋白是参与心脏重塑和心力衰竭的信号通路的重要组成部分。

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  • 作者

    Hongliang Li; rnChengwei He; rnJinhua Feng; rnYan Zhang; rnQizhu Tang; rnZhouyan Bian; rnXue Bai; Heng Zhou; rnHong Jiang; rnScott P. Heximer; rnMu Qin; rnHe Huang; rnPeter. P. Liu; rnCongxin Huang;

  • 作者单位

    Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Physiology, University of Toronto, Toronto, ON, Canada M5S 3J9;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

    rnDivision of Cardiology, Heart and Stroke/Richard Lewar Centre of Excellence, University Health Network, University of Toronto, Toronto, ON, Canada M5S 3E2;

    rnDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China Cardiovascular Research Institute, Wuhan University, Wuhan 430060, China;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    ERK1/2; RGS5; MEK1/2; signal transduction;

    机译：ERK1 / 2;RGS5;MEK1 / 2;信号转导;

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