miR-17-92 ameliorates renal ischemia reperfusion injury

Publication date: Available online 27 October 2017 Source:The Kaohsiung Journal of Medical Sciences Author(s): Turun Song, Mianzhi Chen, Zhengsheng Rao, Yang Qiu, Jinpeng Liu, Yamei Jiang, Zhongli Huang, Xianding Wang, Tao Lin There is limited information on the role of miR-17-92 in renal tubular pathophysiology. Therefore, the present study was performed to determine whether miR-17-92 plays a role in ischemia-reperfusion injury (IRI)-induced acute kidney injury. We originally demonstrated that miR-17-92 is up-regulated following IRI in vivo. To explore the roles of miR-17-92 in the IRI process, we first generated a renal proximal tubule-specific miR-17-92 deletion (PT-miR-17-92−/−) knockout mouse model with Cre driven by the Kap promoter. We found that PT-deficient miR-17-92 mice had more severe renal dysfunction and renal structures than their littermates. Compared with sham-operated mice, both wide-type (WT) mice and PT-miR-17-92−/− mice showed increased serum levels of creatinine and urea. However, the levels of serum urea and creatinine in PT-miR-17-92−/− mice after the IRI operation were significantly higher than the levels in WT mice. In addition, PT-miR-17-92−/− mice showed higher levels of serum potassium and phosphonium after the IRI operation. Histological analysis revealed that PT-miR-17-92−/− mice had substantial histopathologic changes, such as tubular dilation and tubular necrosis. Overexpression of miR-17-92 could partially rev...
Source: The Kaohsiung Journal of Medical Sciences - Category: Universities & Medical Training Source Type: research