Smad3 mediates TGF-β1 induction of VEGF production in lung fibroblasts

Tetsu Kobayashi, Xiangde Liu, Fu Qiang Wen, Qiuhong Fang, Shinji Abe, Xiang Qi Wang, Mitsuyoshi Hashimoto, Lei Shen, Shin Kawasaki, Hui Jung Kim, Tadashi Kohyama, Stephen I. Rennard

Research output: Contribution to journalArticlepeer-review

65 Scopus citations


Transforming growth factor-β1 (TGF-β1) is a key factor in a variety of physiological and pathological processes. Vascular endothelial growth factor (VEGF) is a key angiogenic factor, and vascular change is one of the features of airway remodeling. We examined the effect of TGF-β1 on VEGF production by fibroblasts from mice lacking expression of Smad2 or Smad3 as well as human lung fibroblasts treated with or without Smad2 or Smad3 siRNA. TGF-β1 stimulated VEGF production by fibroblasts from Smad2 deficient animals and wildtype animals. In contrast, TGF-β1 did not affect VEGF production by fibroblasts from Samd3 deficient mice. Similarly, TGF-β1 failed to stimulate VEGF production by HFL-1 cells treated with Samd3 siRNA but significantly increased VEGF production by the cells treated with Smad2 siRNA. These result suggest that TGF-β1 stimulation of VEGF production by fibroblasts is regulated by Smad3 but not by Smad2 signaling.

Original languageEnglish (US)
Pages (from-to)393-398
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Feb 11 2005


  • Smad2
  • Smad3
  • Small interference RNA
  • Transforming growth factor-β1
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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