High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells.

Autor: Huang, Fumeng, Guo, Yuanxu, Wang, Li, Jing, Lanmei, Chen, Zhao, Lu, Shemin, Fu, Rongguo, Tian, Lifang
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Zdroj: Renal Failure; Nov2019, Vol. 41 Issue 1, p762-769, 8p, 2 Charts, 5 Graphs
Abstrakt: There are seven endoplasmic reticulum (ER)-resident selenoproteins in human body and they can regulate the inflammation, oxidative stress, and ER stress. We established transforming growth factor-β1 (TGF-β1) or high glucose (HG) induced human mesangial cells (HMCs) fibronectin expression model in vitro. Next, the expression changes of seven ER-resident selenoproteins were detected under HG conditions and we found selenoprotein S (SELENOS), selenoprotein N (SELENON) were significantly down-regulated but selenoprotein M was significantly up-regulated in transcription level. Furthermore, we found that TGF-β1 and HG down-regulated the expression of SELENOS and SELENON in a time- and dose-dependent manner, respectively. Finally, SELENOS was knocked down by siRNA and we found that knocking down SELENOS decreased TGF-β1 induced fibronectin expression. Our research indicates the potential value of ER-resident selenoproteins on renal fibrosis. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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