Document Detail

Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload.
MedLine Citation:
PMID:  20643937     Owner:  NLM     Status:  MEDLINE    
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 Galphaq and Galphai, 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 transgenic mice with cardiac-specific overexpression of human Rgs5 gene and Rgs5-/- mice. Our results demonstrated that the transgenic 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.
Hongliang Li; Chengwei He; Jinhua Feng; Yan Zhang; Qizhu Tang; Zhouyan Bian; Xue Bai; Heng Zhou; Hong Jiang; Scott P Heximer; Mu Qin; He Huang; Peter P Liu; Congxin Huang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-19
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  107     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-04     Completed Date:  2010-09-08     Revised Date:  2011-07-22    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  13818-23     Citation Subset:  IM    
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
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MeSH Terms
Cardiomegaly / metabolism*,  pathology*
Cells, Cultured
Fibrosis / metabolism
MAP Kinase Signaling System
Mice, Knockout
Organ Specificity
RGS Proteins / deficiency,  genetics,  metabolism*
Stress, Mechanical*
Stress, Physiological*
Reg. No./Substance:
0/RGS Proteins; 0/RGS5 protein, human; 0/Rgs5 protein, mouse

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