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-β1 (transforming growth factor-β1) and α-SMA (α-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, α-SMA and TGF-β1/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-β1/Smad2/3 and subsequently inhibits HLF–MF transition.
Angiotensin-(1–7) decreases the expression of collagen I via TGF-β1/Smad2/3 and subsequently inhibits fibroblast–myofibroblast transition
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Jian Ping Zhou, Wei Tang, Yun Feng, Ning Li, Chen Juan Gu, Qing Yun Li, Huan Ying Wan; Angiotensin-(1–7) decreases the expression of collagen I via TGF-β1/Smad2/3 and subsequently inhibits fibroblast–myofibroblast transition. Clin Sci (Lond) 1 November 2016; 130 (21): 1983–1991. doi: https://doi.org/10.1042/CS20160193
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