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MicroRNA-21 in scleroderma fibrosis and its function in TGF-β-regulated fibrosis-related genes expression.
|Title||MicroRNA-21 in scleroderma fibrosis and its function in TGF-β-regulated fibrosis-related genes expression.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Zhu H, Luo H, Li Y, Zhou Y, Jiang Y, Chai J, Xiao X, You Y, Zuo X|
|Journal||Journal of clinical immunology|
|Date Published||2013 Aug|
Uncontrolled fibrosis in multiple organs is the main cause of death in systemic sclerosis (SSc), and transforming growth factor-β (TGF-β) activation plays a fundamental role in the process. Our previous study demonstrated that miR-21 was significantly up-regulated in SSc fibroblasts. Here, we found that TGF-β regulated the expression of miR-21 and fibrosis-related genes, and decreased Smad7 expression. Over-expression of miR-21 in fibroblasts decreased the levels of Smad7, whereas knockdown of miR-21 increased its expression. Further study using a reporter gene assay demonstrated Smad7 was a direct target of miR-21. Similar to human SSc, the expression of miR-21 increased in the bleomycin induced skin fibrosis. Inhibition of fibrosis by treatment with anti-fibrosis drug bortezomib restored the levels of miR-21 and Smad7. MiR-21 may function in an amplifying circuit to enhance TGF-β signaling events in SSc fibrosis, and suggesting that miR-21 may act as a potential therapeutic target.
|Alternate Journal||J. Clin. Immunol.|