Angiotensin-(1-7) decreases the expression of collagen I via TGF-β1/Smad2/3 and subsequently inhibits fibroblast-myofibroblast transition

作者：Zhou, Jian Ping; Tang, Wei; Feng, Yun; Li, Ning; Gu, Chen Juan; Li, Qing Yun^*; Wan, Huan Ying

来源：Clinical Science, 2016, 130(21): 1983-1991.

DOI：10.1042/CS20160193

• airway remodelling
• angiotensin-(1-7)
• collagen-I
• human lung fibroblast-myofibroblast transition
• Smad2/3
• TGF-beta 1

Previous studies have shown that the RAS (renin-angiotensin system) might participate in airway remodelling in asthma. As a main component of the RAS, Ang-(1-7) [angiotensin-(1-7)] has been reported in few studies regarding its protective effect on asthma. However, the functional roles and relevant signalling pathways of Ang-(1-7) have not been well illustrated. In the present study, we analysed the effect of Ang-(1-7) on AngII (angiotensin II)-induced HLF (human lung fibroblast)-MF (myofibroblast) transition by detecting Col-I (collagen type I), TGF-beta 1 (transforming growth factor-beta 1) and alpha-SMA (alpha-smooth muscle actin) expression. We explored further the possible signalling pathways involved in HLF-MF transition. Our results showed that Ang-(1-7) could down-regulate the expression of Col-I, alpha-SMA and TGF-beta 1/Smad2/3 (all P< 0.05). A significant decrease was found in phosphorylation of PI3K (phosphoinositide 3-kinase), Akt, p38-MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase) signalling pathways during HLF-MF transition (all P< 0.05). Our data suggests that Ang-(1-7) decreases the expression of Col-I via TGF-beta 1/Smad2/3 and subsequently inhibits HLF-MF transition.

• 出版日期2016-11-1
• 单位上海交通大学; 上海市闵行区中心医院