摘要
目的阐明压力负荷诱导的大鼠心脏松弛素受体(relaxin/insulin like family peptide receptor,RXFP1)表达下调的意义及机制。方法利用大鼠主动脉弓结扎(transvers aorta constriction,TAC)方法建立压力负荷模型,Western Blot检测RXFP1表达水平,并检测siRNA敲减RXFP1的乳大鼠成纤维细胞在松弛素作用下胶原的分泌水平。进一步采用Western Blot检测不同浓度TGFβ1孵育乳大鼠心脏成纤维细胞RXFP1的表达变化。结果 TAC组心脏松弛素受体RXFP1表达下调,敲减RXFP1后松弛素抑制乳大鼠心脏成纤维细胞胶原分泌的作用显著减弱,TGFβ1呈剂量依赖性地下调乳大鼠心脏成纤维细胞RXFP1表达。结论在压力负荷诱导的心室重塑模型中,TGFβ1介导了心脏RXFP1下调,并抑制松弛素发挥抗纤维化作用。
Objective To demonstrate cardiac relaxin receptor（relaxin/insulin like family peptide receptor, RXFP1） is down-regulated in the pressure-overload induced ventricular remodeling and its mechanism. Methods Western Blot was used to detect the expression of RXFP1 in the transvers aorta constriction（TAC） rat model. RXFP1 specific siRNA was delivered into neonatal rat cardiac fibroblasts（NRCF） to knock down RXFP1 expression. RXFP1 expression was determined in NRCF treated with different concentration of TGFβ1. Results RXFP1 expression was down regulated in TAC group. By knocking down RXFP1 expression, relaxin could not suppress collagen synthesis in angiotensin II incubated NRCF. TGFβ1 down-regulated RXFP1 expression in a dose-dependent manner. Conclusion TGFβ1 is involved in the down-regulation of cardiac RXFP1 expression in the pressure-overload induced ventricular remodeling, and in turn attenuates the antifibrotic effect of relaxin.
出处
《中国分子心脏病学杂志》
CAS
2014年第3期962-965,共4页
Molecular Cardiology of China
基金
国家自然科学基金(31271212)
