Expression profile of miRNA in chronic kidney disease and identification of miRNA regulating hypoxia and endoplasmic reticulum stress signals

为探讨microRNA（miRNA）在慢性肾脏病（CKD）中的病理生理功能，我们应用microRNA微阵列技术和缺氧诱导的氧化应激内质网（ER）应激对人肾小管上皮细胞（HK-2）进行了功能缺失/获得检测。结果表明：1）缺氧诱导的氧化应激或内质网应激显著降低了miR-205的表达，并与细胞对应激的敏感性相关; 2）PHD 1，其降解转录因子（HIF，ATF 4）的缺氧和内质网应激信号，是miR-205的靶点，3）降低miR-205抑制HIF/ATF 4下游基因，抗氧化酶，通过上调PHD 1。miR-205可能有助于肾小管稳态。

To assess the pathophysiological function of microRNA (miRNA) inchronic kidney disease (CKD), we performed the miRNA microarray analysis and the loss/gainfunction assay in human tubular cells (HK-2) expose to hypoxia-induced oxidative stressor endoplasmic reticulum (ER) stress. The results demonstrated that 1) miR-205 expressionwas significantly decreased by hypoxia-induced oxidative stress or ER stress and wasassociated with cellular sensitivity to the stresses, 2) PHD1, which degradestranscription factors (HIF, ATF4) of hypoxia and ER stress signals, is a target for miR-205,3) decreased miR-205 suppressed the expression of HIF/ATF4 downstream genes, anti-oxidantenzymes, via upregulation of PHD1. miR-205 might contribute to tubular homeostasis.