MiR-150 Regulates Mesenchymal Stem Cells Migration To Diabetic Nephropathy By CXCR4

Objective: To study the mi R-150 regulates Mesenchymal stem cells migration to diabetic nephropathy through CXCR4 / SDF-1.Method: Flow cytometry was used to evaluate the CD phenotypes on the surface of MSCs. Adipogenic and osteogenic differentiations of MSCs were detected by fluorescence microscopy. Real-time RT-PCR was used to detect the expression of mi R-150 in MSCs. Transwell migration experiment detected MSCs migration. Also, the expressions of CXCR4, SDF-1and E-Ca were tested by western blot. The levels of blood glucose, 24-h urine protein, and creatinine clearance were measured. The pathological changes in the renal tissues were examined by HE.Result : MSCs expressed positively the CD29(97±2.25), CD90(99±0.6%),and negatively the CD45(17±4.5). MSCs had the potency of differentiating into fat, bone cells. The expression of mi R-150 in MSCs was reduced in DN compared with normal group(p﹤0.05). Also, the expressions of CXCR4 and SDF-1 were increased in DN(p﹤0.05). The expressions of CXCR4 and SDF-1 were declined in mi R-150 over-expressed MSCs(p﹤0.05). Moreover, the number of MSCs migration were increased in mi R-150 inhibitor compared with control group. Compared with the DN group, the mi R-150 inhibitor-MSC showed decreased levels of blood glucose, 24-h urine protein, kidney weight index and improved renal histopathology(p﹤0.05). In the renal tissue, the CXCR4 and SDF-1 were increased in DN compared with normal group(p﹤0.05). However, the expression of CXCR4 and SDF-1 proteins were reduced in mi R-150 inhibitor-MSC compared with DN group(p﹤0.05).Conclusion:Knockdown mi R-150 have caused CXCR4 expression increased, thus stimulate MSCs homing, thereby improve the damaged kidney tissue.