Smad3 deficiency attenuates bleomycin-induced pulmonary fibrosis in mice.

Journal Article (Journal Article)

Transforming growth factor-beta (TGF-beta) signaling plays an important regulatory role during lung fibrogenesis. Smad3 was identified in the pathway for transducing TGF-beta signals from the cell membrane to the nucleus. Using mice without Smad3 gene expression, we investigated whether Smad3 could regulate bleomycin-induced pulmonary fibrosis in vivo. Mice deficient in Smad3 demonstrated suppressed type I procollagen mRNA expression and reduced hydroxyproline content in the lungs compared with wild-type mice treated with bleomycin. Furthermore, loss of Smad3 greatly attenuated morphological fibrotic responses to bleomycin in the mouse lungs, suggesting that Smad3 is implicated in the pathogenesis of pulmonary fibrosis. These results show that Smad3 contributes to bleomycin-induced lung injury and that Smad3 may serve as a novel target for potential therapeutic treatment of lung fibrosis.

Full Text

Duke Authors

Cited Authors

  • Zhao, J; Shi, W; Wang, Y-L; Chen, H; Bringas, P; Datto, MB; Frederick, JP; Wang, X-F; Warburton, D

Published Date

  • March 2002

Published In

Volume / Issue

  • 282 / 3

Start / End Page

  • L585 - L593

PubMed ID

  • 11839555

International Standard Serial Number (ISSN)

  • 1040-0605

Digital Object Identifier (DOI)

  • 10.1152/ajplung.00151.2001


  • eng

Conference Location

  • United States