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. 2016 Oct 17;5(10):e003910. doi: 10.1161/JAHA.116.003910

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© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Endogenous SO ₂ inhibited the Smad2/3 signaling pathway and collagen deposition. A, AAT1 protein expression, SO ₂ content, and AAT activity in PAFs overexpressing AAT1. B, The phosphorylation of Smad2/3 induced by TGF‐β1 in PAFs overexpressing AAT1. C and D, Western blotting (C) and immunofluorescence analysis (D) of collagen types I and III induced by TGF‐β1 in PAFs with AAT1 overexpression. Results are expressed as mean±SE for 3 separate experiments (n=3), each in triplicate. *P<0.05 compared with the vehicle group; ^# P<0.05 compared with the vehicle plus TGF‐β1 group. AAT1 indicates aspartate aminotransferase 1; PAF, pulmonary arterial fibroblast; SO₂, sulfur dioxide; TGF‐β1, transforming growth factor β1.