Plasminogen activator inhibitor-I-related regulation of procollagen I (α1 and α2) by antitransforming growth factor-β1 treatment during radiation-impaired wound healing

Conclusion: These results emphasize anti-TGF-β1 treatment to reduce radiation-induced fibrosis by decreasing α1(I)-procollagen synthesis in vivo. α1(I)-procollagen and α2(I)-procollagen might be differentially regulated by anti-TGF-β1 treatment. Increased TGF-β signaling in irradiated skin fibroblasts seemed to be reversible, as shown by a reduction in PAI-1 expression after anti-TGF-β1 treatment.