The Krüppel-like factor 15 inhibits myocardial fibrosis in a rat model of left ventricular pressure overload / 中华胸心血管外科杂志

ABSTRACT

Objective Based on animal model of left ventricular pressure overload induced cardiac fibrosis,to investigate the specific role and molecular mechanism of KLF15 gene in this process.Methods To establish rat animal model of pressure overload induced cardiac hypertrophy by aortic coarctation under non artificial ventilation conditions,and then release the constriction,to observe the rat heart color Doppler images,myocardial interstitial fibrosis features and protein expression level changes of KLF15、Transforming growth factor-β (TGF-β) 、Connective tissue growth factor (CTGF)、Myocardin-related transcription factor A(MRTF-A) in overload-unload corresponding time points.Results We successfully completed aortic banding and debanding operations by use of SD rats without artificial ventilation.Through color Doppler echocardiography detection,from images to knowthe effect of constriction and loosening is definite.The expression of collagen type Ⅰ,collagen type Ⅲ,TGF-β,CTGF,MRTF-A were significantly higher and myocardial hypertrophy was aggravated but the KLF15 protein expression level was significantly lower in pressure overloaded rats than in Sham rats(all P ＜ 0.05).All values were in an increasing tendency with the constrictive time prolonged (P ＜ 0.05).The response to unloading was opposite,the sooner to loose the better to the recovery to normal.The differences of indicators are very notable (P ＜ 0.05).Conclusion By feedback regulation TGF-β,KLF15 inhibited the effect of CTGF and MRTF-A,reducing myocardial interstitial fibrosis.