• Zhonghua yi xue za zhi · Oct 2017

    [The role of estrogen related-receptor γ and ATP-dependent K(+) channel Kcnj1 in renal ischemia-reperfusion injury].

    • Z M Wu, Q Yang, Z Y Li, D Chen, L J Jiang, X D Li, S L Chen, and Z W Liu.
    • Department of Urology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
    • Zhonghua Yi Xue Za Zhi. 2017 Oct 17; 97 (38): 3017-3021.

    AbstractObjective: To investigate the correlation between estrogen related-receptorγ (ERRγ) and ATP-dependent K(+) channel Kcnj1 in renal ischemia-reperfusion injury and its possible role in regulating ischemic preconditioning. Methods: The expression of ERRγ in kidney tissues was detected by immunohistochemistry. The expressions of ERRγ and Kcnj1 in human renal tubular epithelial cells (HK-2) under hypoxia (1% O(2)) were detected by RT-PCR. The ERRγ-deficient heterozygous mice model and the ERRγ-deficient completely mice model were established. The pretreatedischemia-reperfusion model were constructed in wild-type mice, ERRγ-deficient heterozygous mice and ERRγ-deficient completely mice, respectively. Renal injury was observed under a light microscope with PAS staining. ERRγ and Kcnj1 were tested by immunohistochemistry and RT-PCR. Results: ERRγ in mice kidney tissue was mainly expressed in renal tubules, and the expressions of ERRγ and Kcnj1 were decreased 59% and 29.5% respectively after hypoxia in the renal tubular cells (HK-2). In the animal model, the expressions of ERRγ and Kcnj1 were decreased 31.9% and 11% in early ischemic mice kidney tubular cells of wild type. The expressions of ERRγ and Kcnj1 in renal tubular cells were decreased 33.2% and 19.1% after ischemia and reperfusion. When ERRγ were overexpressed in renal tubular cells, ERRγ was increased by 89%, and the expression of Kcnj1 was increased by 72.5%. The expression of Kcnj1 was decreased by 75.7% in ERRγ-deficient completely mice. However, Kcnj1 expression in renal tissue of ERR-γ-deficient mice was stable, but ischemic preconditioning failed to interfere with renal ischemia-reperfusion injury. Conclusion: ERRγ-Kcnj1 is closely related to ischemic preconditioning and protects renal ischemia-reperfusion injury, and may be one of the regulatory factors. To explore the protective effect of the regulating pathway on ischemia reperfusion injury couldprovide a theoretical basis for the development of drug pretreatment.

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