FK506 inhibits the mice glomerular mesangial cells proliferation by affecting the transforming growth factor-β and Smads signal pathways. (May 2014)

• Record Type: Journal Article
• Authors: Qi, Ren; Li, Wen; Yu, Shengyou
• Is Part Of: Renal failure. Volume 36:Number 4(2014)
• Page Start: 589
• Page End: 592
• Publication Date: 2014-05
• Subjects: Chronic renal failure -- Periodicals; Acute renal failure -- Periodicals; Uremia -- Periodicals; 616.614005
• DOI: 10.3109/0886022X.2014.882713
• Languages: English
• ISSNs: 0886-022X

Abstract

<abstract> <title>Abstract</title> <p>TGF-β1 plays an important role in the pathogenesis of chronic renal diseases. Although the specific mechanism is unknown, a major factor is the potent fibrogenic activity of TGF-β1 in the chronic progression of renal diseases. TGF-β1 closely correlates with renal fibrosis in cooperation with several fibrosis-promoting molecules. Recently it has been studied that, Smad proteins as intracellular mediators of TGF-β signaling pathways provide important insights into the mechanisms determining the specificity of TGF-β action in various renal cells. Some studies have proved that immunosuppressants can affect TGF-β expression, but the mechanisms are unclear. In this study, we investigated the effect of FK506 on mesangial cells via TGF-β and Smads signal pathways. Our results shows that FK506 effectively blocked the TGF-β/Smad signaling pathway by downregulation of TGF-β receptor, and played an important role in TGF-β1-induced Smad2 expression in mice mesangial cells. FK506 can inhibit the TGF-β1-stimulated cell proliferation via Smad-related pathways. And reduced the Smad2 protein and mRNA expression. Altogether, this study provided a theoretical proof for the protective and treating effect of FK506 on kidneys.</p> </abstract>