Erythropoietin Inhibits Hypoxia–Induced Epithelial-To-Mesenchymal Transition via Upregulation of miR-200b in HK-2 Cells

• Main Authors: Jiuxu Bai, Xiao Xiao, Xiaoling Zhang, Hanmin Cui, Junfeng Hao, Jingming Han, Ning Cao
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2017-05-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Erythropoietin; miR-200b; Endothelial-to-mesenchymal transition; Renal tubular
• Online Access: http://www.karger.com/Article/FullText/477327

Background/Aims: Renal tubular epithelial-mesenchymal transition (EMT) is regarded as an important factor leading to renal interstitial fibrosis. Erythropoietin (EPO) has been reported to attenuate renal fibrosis. The mechanism underlying this protective effect of EPO remains unclear. In this study, we aim to identify possible mechanisms of the EPO renoprotective effect. Methods: Hypoxia was induced in vitro by incubating human proximal tubular epithelial cell line HK-2 cells in 1% O2 and 5% CO2. Western blotting and reverse transcription polymerase chain reaction analyses were used to evaluate the expression of epithelial and mesenchymal markers in the cell samples. The expression of miR-200b in the HK-2 cells under hypoxia or treatment with EPO was examined. Results: EPO represses hypoxia-induced EMT by upregulating miR-200b in HK-2 cells. Overexpression of miR-200b represses the effect of ETS proto-oncogene 1 (Ets-1)-induced EMT in HK-2 cells. Conclusion: miR-200 mediates the protective effects of EPO on EMT in hypoxic HK-2 cells. EPO attenuated hypoxia-induced EMT by increasing miR-200 expression via the repression of Ets-1.