Effects of short-chain acyl-CoA dehydrogenase on collagen expression and proliferation of rat cardiac fibroblasts
10.3969/j.issn.1000-4718.2016.12.010
- VernacularTitle:短链酰基辅酶A脱氢酶在心脏成纤维细胞胶原表达和细胞增殖中的作用
- Author:
Zhaohui SHU
;
Zhenhua ZENG
;
Qiuju HUANG
;
Zhonghong LI
;
Peiqing LIU
;
Shaorui CHEN
;
Tian LAN
;
Linquan ZANG
;
Sigui ZHOU
- Keywords:
Short-chain acyl-CoA dehydrogenase;
Cardiac fibroblasts;
Myocardial fibrosis;
Energy metabo-lism;
Collagen
- From:
Chinese Journal of Pathophysiology
2016;32(12):2184-2191
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .
