全反视黄酸调节心脏特异转录因子蛋白表达及其机制  

Inhibition of dHAND expression by atRA in H9c2 cells and its mechanism

作　　者：李卫新[1] 李勇[1] 

机构地区：[1]北京大学公共卫生学院营养与食品卫生学系,北京100083

出　　处：《中国生育健康杂志》2006年第1期34-37,共4页Chinese Journal of Reproductive Health

基　　金：国家自然科学基金资助项目(No.30371208)

摘　　要：目的探讨全反视黄酸(atRA)对心脏特异转录因子(dHAND)蛋白表达的调节作用和分子机制。方法用atRA处理H9c2细胞,然后用Western blot分析和免疫组化方法来检测dHAND表达。结果在H9c2细胞中,atRA可抑制dHAND蛋白表达,这一抑制作用具有时间和剂量依赖性。Western blot分析和免疫组化检测均证实,5μnol／L 的atRA处理H9c2细胞2h可以显著降低dHAND和ET-1蛋白的表达。用BQ-123阻断ET -1／ETAR信号通路后,dHAND表达上调。结论在H9c2细胞中,atRA通过ET-1／ ETAR信号传导通路来抑制dHAND表达。Objective To explore the regulation of atRA to dHAND protein expression in H9c2 cells and its mechanism. Methods Protein level of dHAND was measured after the atRA treatment by western blot analysis and immunohistochemical assay. Results atRA inhibited the expression of dHAND protein in H9c2 cells in a time and dose dependent manner. 5 μmol/L atRA treatment for 2h reduced the protein expression levels of dHAND and ET-1. dHAND protein level was increased after the blockade of ET-1/ETAR signaling pathway by BQ-123. Conclusion atRA suppresses the dHAND protein expression via ET-1/ETAR signaling in H9c2 cells.

关 键 词：心脏发育 全反视黄酸 心脏特异转录因子 内皮素-1 信号传导 

分 类 号：R541[医药卫生—心血管疾病]