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Effect of intermedin1-53 on aldosterone-induced cardiac fibroblast proliferation
Authors:XUE Li-hua  LIANG Ying  SONG Jun-qiu  QI Yong-fen  JIA Yue-xia
Institution:1. Department of Pathophysiology,School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China; 2. Department of Physiology and Pathophysiology,Peking University Health Science Center, Beijing 100083, China
Abstract:AIM: To investigate the roles of intermedin1-53 (IMD1-53) and exteracellular signal-regulated kinase (ERK) signal pathway in the proliferation of rat cardiac fibroblasts (CFBs).METHODS: Isolated and cultured CFBs from new born SD rats were randomly divided into control group, aldosterone (ALD) groups (at different concentrations) and ALD+IMD groups (IMD at different concentrations). The viability of CFBs was determined by MTT assay. Western blotting was used to observe the effect of IMD on ALD-induced ERK phosphorylation.RESULTS: IMD1-53 had no significant effect on the proliferation of CFBs in basal state, but inhibited the CFBs growth stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner. IMD1-53 also inhibited ERK phosphorylation stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner.CONCLUSION: IMD1-53 inhibits the proliferation of CFBs by ERK signal pathway.
Keywords:Intermedin1-53  Cardiac fibroblast  Aldosterone  ERK pathway  
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