Title : Thalidomide inhibits fibronectin production in TGF-β1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway.

Pub. Date : 2013 Jun 1

PMID : 23500539






5 Functional Relationships(s)
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1 Thalidomide inhibits fibronectin production in TGF-beta1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway. Thalidomide fibronectin 1 Homo sapiens
2 The aims were to examine possible therapeutic effects of thalidomide on fibronectin expression in transforming growth factor-beta1 (TGF-beta1)-treated normal fibroblasts (NFs) and keloid-derived fibroblasts (KFs) and the underlying mechanism of action, especially the involvement of mitogen-activated protein kinase (MAPKs) and Sma- and Mad-related family (Smads) pathways. Thalidomide fibronectin 1 Homo sapiens
3 TGF-beta1 induced significant fibronectin expression in NFs and KFs and the effect was inhibited by pretreatment with thalidomide. Thalidomide fibronectin 1 Homo sapiens
4 In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model. Thalidomide fibronectin 1 Homo sapiens
5 In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model. Thalidomide fibronectin 1 Homo sapiens