Smad3 mediates TGF-beta1 induction of VEGF production in lung fibroblasts |
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Authors: | Kobayashi Tetsu Liu Xiangde Wen Fu-Qiang Fang Qiuhong Abe Shinji Wang Xiang Qi Hashimoto Mitsuyoshi Shen Lei Kawasaki Shin Kim Hui Jung Kohyama Tadashi Rennard Stephen I |
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Affiliation: | University of Nebraska Medical Center, Omaha, NE, USA. |
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Abstract: | Transforming growth factor-beta1 (TGF-beta1) 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-beta1 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-beta1 stimulated VEGF production by fibroblasts from Smad2 deficient animals and wildtype animals. In contrast, TGF-beta1 did not affect VEGF production by fibroblasts from Samd3 deficient mice. Similarly, TGF-beta1 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-beta1 stimulation of VEGF production by fibroblasts is regulated by Smad3 but not by Smad2 signaling. |
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Keywords: | Small interference RNA Smad2 Smad3 Transforming growth factor-β1 Vascular endothelial growth factor |
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