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HMGB1 induces lung fibroblast to myofibroblast differentiation through NF­κB­mediated TGF­ß1 release.

Mol Med Rep; 15(5): 3062-3068, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28339089
The proinflammatory factor high­mobility group box protein 1 (HMGB1) has been implicated in the pathogenesis of lung fibrosis; however, the role of HMGB1 in lung fibrosis remains unclear. It has previously been reported that nuclear factor (NF)­κB and transforming growth factor (TGF)­ß1 may be involved in lung fibrosis. Therefore, the present study aimed to examine the potential molecular mechanisms that underlie HMGB1­induced lung fibrosis via the regulation of NF­κB and TGF­ß1. The results demonstrated that HMGB1 stimulation increased the activation of NF­κB and the release of TGF­ß1, as well as the expression of α­smooth muscle actin (α­SMA) and collagen I in human lung fibroblasts in vitro. In addition, inhibition of NF­κB activation blocked HMGB1­induced TGF­ß1 release, as well as α­SMA and collagen I expression in lung fibroblasts. Preventing the release of TGF­ß1 inhibited HMGB1­induced α­SMA and collagen I expression; however, it had no effect on NF­κB activation. Collectively, these findings indicate that HMGB1 induces fibroblast to myofibroblast differentiation of lung fibroblasts via NF­κB­mediated TGF­ß1 release.