Effect of miR-190a-3P on Chronic Diabetic Nephropathy by Regulating FGFR3

Chronic diabetic nephropathy (CDN) is one of the common complications of the chronic diabetes. The FGF23/FGFR3-mediated signaling pathway is involved in CDN. Whether miR-190a-3P participates in CDN through regulation of FGFR3 remains to be elucidated. The present study evaluated miR-190a-3P's effect on CDN.

Mice were divided into a control group (NC group), a CDN group, and CDN+miR-190a-3P antagonist group, followed by analysis of miR-190a-3P and FGFR3 level by qRT-PCR, FGFR3, and Tubulin protein level by Western blot as well as blood glucose, serum creatinine (Cr), and urea nitrogen (BUN) using an automatic biochemical analyzer.

Compared with the NC group, the CDN group had a significantly higher miR-190a-3P level in kidney tissue, while the FGFR3 mRNA level was lower (P<0.01). FGFR3 was a target gene of miR-190a-3P. miR-190a-3P levels in the CDN+miR-190a-3P antagonist group were significantly reduced compared with the CDN group (P<0.05). Meanwhile, FGFR3 protein levels in miR-190a-3P antagonist group were significantly increased (P<0.05). Compared with the NC group, the CDN group showed significantly reduced blood glucose level and elevated BUN and Cr level (P<0.01). However, CDN+miR-190a-3P antagonist group showed significantly increased blood glucose and reduced BUN and Cr level compared with CDN group (P<0.05).

miR-190a-3P can directly bind to the 3'-UTR of FGFR3 mRNA and reduce FGFR3 protein levels, contributing to the occurrence of CDN.