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| Research article summary (published 20 May 2009): |
The linker region of Smad2 mediates TGF-beta-dependent ERK2-induced collagen synthesis.
Full Abstract
Transforming growth factor (TGF)-beta1 can cause fibrosis diseases by enhancing production of collagen. However, the intracellular signaling mechanism for TGF-beta1 stimulation of this process has not been fully elucidated. The present study focused on this mechanism and the cross-talk between the MAPK and Smad pathways. Extracellular signal-regulated kinase (ERK)2 ablation by a small interfering RNA led to marked inhibition of TGF-beta1-induced collagen synthesis and enhanced phosphorylation of the Smad2 linker site in NIH/3T3 fibroblast cells. However, ERK1 ablation had minimal effects. Ablation of either ERK2 or ERK1 had no effect on the phosphorylation of the Smad2 C-terminal site. Furthermore, a Smad2 mutant with reduced phosphorylation of the Smad2 linker site inhibited TGF-beta1-induced collagen synthesis. These results indicate that ERK2, rather than ERK1, plays a predominantly positive role in TGF-beta1-induced collagen synthesis, and that ERK2 enhances collagen synthesis, at least partially, through activation of the Smad2 linker site.
Author information
Author/s: Li, Fengfeng (F); Zeng, Bingfang (B); Chai, Yimin (Y); Cai, Peihua (P); Fan, Cunyi (C); Cheng, Tao (T);
Affiliation: Department of Orthopaedics, The Sixth Affiliated People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200233, China.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), published in United States. (Language: eng)
Reference: 2009-Aug; vol 386 (issue 2) : pp 289-93
Dates: Created 2009/07/06; Completed 2009/07/27;
PMID: 19465000, status: MEDLINE (last retrieval date: 8/20/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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