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

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. 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. 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. 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.