Yuan Lin, Chaoyan Yin, Yanjing Liu, Donghui Lu, Xiaofen Lian
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引用次数: 0
Abstract
Objective: 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.
Methods: 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.
Results: 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).
Conclusion: miR-190a-3P can directly bind to the 3'-UTR of FGFR3 mRNA and reduce FGFR3 protein levels, contributing to the occurrence of CDN.
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