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Am J Physiol Lung Cell Mol Physiol (October 26, 2001). doi:10.1152/ajplung.00151.2001
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Articles in PresS, published online ahead of print October 26, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00151.2001
Submitted on April 28, 2001
Accepted on October 22, 2001

Smad3 Deficiency Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

Jingsong Zhao1*, Wei Shi2, Yan-Ling Wang1, Hui Chen1, Pablo Bringas Jr.1, Michael B Datto3, Joshua P Frederick3, Xiao-Fan Wang3, and David Warburton2

1 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA
2 Dept. of Surgery and Pediatrics, and the Cell and Developmental Biology Program, The Childrens Hospital Los Angeles Research Institute, Los Angeles, CA, USA
3 Dept. of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: jingsongzhao{at}yahoo.com.

Transforming growth factor-ß (TGF-ß) signaling plays an important regulatory role during lung fibrogenesis. Smad3 was identified in the pathway for transducing TGF-ß 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 in comparison to 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.




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