Previous studies have shown that renin-angiotensin system (RAS) might participate in airway remodeling in asthma. As a main component in RAS, Angiotensin-(1-7) [Ang-(1-7)] has been reported in few studies regarding its protective effect on asthma. However, the functional roles and relevant signaling pathways of Ang-(1-7) have not been well illustrated. In the present study, we analyzed the effect of Ang-(1-7) on Angiotensin II (AngII)-induced human lung fibroblast (HLF)-myofibroblast (MF) transition by detecting collagen type I (Col-I), transforming growth factor-beta 1(TGF-β1) and α-smooth muscle actins (α-SMA) expression. We further explored the possible signaling pathways involved in HLF-MF transition. Our results showed that Ang-(1-7) could downregulate 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, Akt, p38-MAPK and JNK signaling 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.
- Airway remodeling
- HLF-MF transition
- ©2016 The Author(s)
This is an Accepted Manuscript; not the final Version of Record. You are encouraged to use the final Version of Record that, when published, will replace this manuscript and be freely available under a Creative Commons licence.