Increased expression and activation of serum- and glucocorticoid-inducible kinase-1 (SGK1) by cadmium in HK-2 renal proximal tubular epithelial cells

被引：5

作者：

Miyayama, Takamitsu ^{[1
]}

Matsuoka, Masato ^{[1
]}

机构：

[1] Tokyo Womens Med Univ, Dept Hyg & Publ Hlth 1, Shinjuku Ku, Tokyo 1628666, Japan

来源：

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2014年 / 38卷 / 02期

基金：

日本学术振兴会;

关键词：

Cadmium; SGK1; NDRG1; EMD638683; HK-2; cells; PROTEIN-KINASE; PHOSPHORYLATION; SURVIVAL; ISOFORMS; PATHWAY;

D O I：

10.1016/j.etap.2014.07.004

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

In HK-2 cells exposed to cadmium chloride (CdCl2), the level of serum- and glucocorticoid-inducible kinase-1 (SGK1) protein is increased, but the levels of SGK2 and SGK3 proteins are not. Phosphorylation of SGK1 protein is also observed. Treatment with actinomycin D abolished CdCl2-induced elevation of SGK1 mRNA level. Treatment with actinomycin D or cycloheximide suppressed SGK1 protein levels in cells exposed to CdCl2. Treatment with SGK1 inhibitor EMD638683 or knockdown of SGK1 with siRNA suppressed CdCl2-induced phosphorylation of N-Myc downstream-regulated kinase 1 (NDRG1). These results indicate that cadmium induces the transcriptional upregulation of SGK1 expression and regulates NDRG1 in HK-2 cells. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：374 / 378

页数：5

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