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

被引：11
|
作者：
Huang, Fumeng [1 ]
Guo, Yuanxu [2 ]
Wang, Li [1 ]
Jing, Lanmei [1 ]
Chen, Zhao [1 ]
Lu, Shemin [2 ]
Fu, Rongguo [1 ]
Tian, Lifang [1 ]
机构：
[1] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Nephrol, Xian 710004, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Coll Med, Dept Genet & Mol Biol, Xian, Shaanxi, Peoples R China
来源：
RENAL FAILURE | 2019年 / 41卷 / 01期
基金：
中国国家自然科学基金;
关键词：
Endoplasmic reticulum; selenoprotein S; selenoprotein N; HMCs; glucose; TGF-beta; 1; GENE-EXPRESSION; STRESS; ACTIVATION; SEPS1; ROLES; SELS;
D O I：
10.1080/0886022X.2019.1641413
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
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-beta 1 (TGF-beta 1) 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-beta 1 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-beta 1 induced fibronectin expression. Our research indicates the potential value of ER-resident selenoproteins on renal fibrosis.
引用
收藏
页码：762 / 769
页数：8
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