| Literature DB >> 12589683 |
Xiangde Liu1, Fu-Qiang Wen, Tetsu Kobayashi, Shinji Abe, Qiuhong Fang, Ester Piek, Erwin P Bottinger, Anita B Roberts, Stephen I Rennard.
Abstract
TGF-beta signals through TGF-beta receptors and Smad proteins. TGF-beta also augments fibroblast-mediated collagen gel contraction, an in vitro model of connective tissue remodeling. To investigate the importance of Smad2 or Smad3 in this augmentation process, embryo-derived fibroblasts from mice lacking expression of Smad2 or Smad3 genes were cast into native type I collagen gels. Fibroblast-populated gels were then released into 0.2% FCS-DMEM alone or with recombinant human TGF-beta1, beta2, beta3, or recombinant rat PDGF-BB. Gel contraction was determined using an image analyzer. All three isoforms of TGF-beta significantly augmented contraction of collagen gels mediated by fibroblasts with genotypes of Smad2 knockout (S2KO), Smad2 wildtype (S2WT), and Smad3 wildtype (S3WT), but not Smad3 knockout (S3KO) mice. PDGF-BB augmented collagen gel contraction by all fibroblast types. These results suggest that expression of Smad3 but not Smad2 may be critical in TGF-beta augmentation of fibroblast-mediated collagen gel contraction. Thus, the Smad3 gene could be a target for blocking contraction of fibrotic tissue induced by TGF-beta. Copyright 2003 Wiley-Liss, Inc.Entities:
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Year: 2003 PMID： 12589683 DOI： 10.1002/cm.10098
Source DB: PubMed Journal: Cell Motil Cytoskeleton ISSN： 0886-1544