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目的研究高糖诱导的心肌间质纤维化(心肌成纤维细胞表型转化以及胶原分泌)过程中活化素受体样激酶7(ALK7)的作用。方法体外高糖培养大鼠心肌成纤维细胞,免疫荧光法观察成纤维细胞表型转化,real time-PCR法检测心肌成纤维细胞ALK7和Ⅰ型前胶原mRNA的表达水平,ELISA法检测心肌成纤维细胞分泌Ⅰ型胶原水平,Western-blotting法测定心肌成纤维细胞ALK7蛋白的表达水平;siRNA抑制ALK7表达,再次观察高糖对心肌成纤维细胞表型转化及上述各因子表达的影响。结果高糖刺激心肌成纤维细胞转化为肌成纤维细胞;高糖促进Ⅰ型胶原mRNA和蛋白的表达(P<0.05);高糖促进成纤维细胞ALK7 mRNA和蛋白的表达(P<0.05);ALK7 siRNA抑制ALK7的表达后,高糖促进心肌成纤维细胞转化及合成Ⅰ型胶原的作用下降(P<0.05)。结论 ALK7参与了高糖诱导的心肌成纤维细胞表型转化及合成Ⅰ型胶原的代谢过程。
Objective To investigate the role of activin receptor-like kinase 7 (ALK7) during hyperglycemia-induced myocardial interstitial fibrosis (phenotypes of cardiac fibroblasts and collagen secretion). Methods Cardiac fibroblasts were cultured with high glucose in vitro. The phenotypic changes of fibroblasts were observed by immunofluorescence. The mRNA expression of ALK7 and type Ⅰ procollagen in cardiac fibroblasts was detected by real time-PCR. The myocardial fibrosis The cells secreted type I collagen. The expression of ALK7 protein in cardiac fibroblasts was detected by Western-blotting. SiRNA inhibited the expression of ALK7 and observed the effect of high glucose on the phenotype of cardiac fibroblasts and the expression of these factors. Results High glucose stimulated myofibroblasts to transform into myofibroblasts. High glucose promoted the expression of type Ⅰ collagen mRNA and protein (P <0.05). High glucose promoted the expression of ALK7 mRNA and protein in fibroblasts (P <0.05). After ALK7 siRNA inhibited ALK7 expression, the effect of high glucose on cardiac fibroblast transformation and synthesis of type I collagen decreased (P <0.05). CONCLUSIONS: ALK7 is involved in the phenotypic transformation of cardiac fibroblasts induced by high glucose and the metabolic process of synthesizing type I collagen.