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

  • Environ Toxicol Pharmacol. 2014 Sep;38(2):374-8. doi: 10.1016/j.etap.2014.07.004.
Takamitsu Miyayama  1 ,  Masato Matsuoka  2
Affiliations
  • 1. Department of Hygiene and Public Health I, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
  • 2. Department of Hygiene and Public Health I, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan. Electronic address: [email protected].
PMID: 25128767 DOI: 10.1016/j.etap.2014.07.004
Abstract

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.

Keywords
Cadmium; EMD638683; HK-2 cells; NDRG1; SGK1.
Products