| First Author | Song T | Year | 2018 |
| Journal | Kaohsiung J Med Sci | Volume | 34 |
| Issue | 5 | Pages | 263-273 |
| PubMed ID | 29699633 | Mgi Jnum | J:272165 |
| Mgi Id | MGI:6282623 | Doi | 10.1016/j.kjms.2017.09.003 |
| Citation | Song T, et al. (2018) miR-17-92 ameliorates renal ischemia reperfusion injury. Kaohsiung J Med Sci 34(5):263-273 |
| abstractText | 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 reverse the side-effects of IRI on the proximal tubules in vivo. Furthermore, we employed a quantitative proteomic strategy and identified 16 proteins as potential targets of miR-17-92. Taken together, our findings suggested that miR-17-92 may ameliorates IRI-induced acute kidney injury. Our results indicate that pharmacologic modulation of these miRNAs may have therapeutic potential for acute kidney injury. |
