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1 Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles 90033; 2 Departments of Surgery and Pediatrics, and the Cell and Developmental Biology Program, The Childrens Hospital Los Angeles Research Institute, Los Angeles, California 90027; and 3 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710
Transforming growth factor-
(TGF-)
signaling plays an important regulatory role during lung fibrogenesis.
Smad3 was identified in the pathway for transducing TGF- 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.
transforming growth factor-; hydroxyproline
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