Increased expression and activation of serum- and glucocorticoid-inducible kinase-1 (SGK1) by cadmium in HK-2 renal proximal tubular epithelial cells
Increased expression and activation of serum- and glucocorticoid-inducible kinase-1 (SGK1) by cadmium in HK-2 renal proximal tubular epithelial cells
复制标题
镉在 HK-2 肾近端肾小管上皮细胞中增加血清和糖皮质激素诱导激酶 1 (SGK1) 的表达和激活
DOI：
10.1016/j.etap.2014.07.004
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发表时间：
2014
影响因子：
4.3
通讯作者：
Matsuoka M
中科院分区：
文献类型：
--
作者：
Miyayama T;Matsuoka M
在暴露于氯化镉（CdCl2）的HK-2细胞中，血清和糖皮质激素诱导激酶-1 （SGK1）蛋白水平升高，但SGK2和SGK3蛋白水平未升高。SGK1蛋白的磷酸化也被观察到。放线菌素D可消除cdcl2诱导的SGK1 mRNA水平升高。放线菌素D或环己亚胺治疗可抑制CdCl2暴露细胞中的SGK1蛋白水平。使用SGK1抑制剂EMD638683或用siRNA敲低SGK1可抑制cdcl2诱导的N-Myc下游调节激酶1 （NDRG1）的磷酸化。这些结果表明，在HK-2细胞中，镉诱导SGK1表达上调并调控NDRG1。
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.