Smad3 mediates the TGF-β-induced contraction of type I collagen gels by mouse embryo fibroblasts

Xiangde Liu, Fu Qiang Wen, Tetsu Kobayashi, Shinji Abe, Qiuhong Fang, Ester Piek, Erwin P. Bottinger, Anita B. Roberts, Stephen I. Rennard

Research output: Contribution to journalArticlepeer-review

41 Scopus citations


TGF-β signals through TGF-β receptors and Smad proteins. TGF-β 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-β1, β2, β3, or recombinant rat PDGF-BB. Gel contraction was determined using an image analyzer. All three isoforms of TGF-β 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-β augmentation of fibroblast-mediated collagen gel contraction. Thus, the Smad3 gene could be a target for blocking contraction of fibrotic tissue induced by TGF-β.

Original languageEnglish (US)
Pages (from-to)248-253
Number of pages6
JournalCell Motility and the Cytoskeleton
Issue number3
StatePublished - Mar 1 2003


  • Knockout mice
  • Smad
  • Tissue remodeling

ASJC Scopus subject areas

  • Structural Biology
  • Cell Biology


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