Diabetic kidney disease (DKD) is a leading cause of chronic and end-stage renal failure in the world. However, the underlying molecular mechanisms are various and not completely understood. In our previous study, miR-223-3p was identified as the most significantly decreased miRNAs and showed a disease-dependent expression in the plasma of DKD patients through microarray analysis, which was involved in biological processes, such as cell proliferation, differentiation, apoptosis and immune regulation. In the present study, we firstly used high glucose stimulation to establish human umbilical vein endothelial cells (HUVECs) injury in vitro DKD model and db/db mice in vivo DKD model, respectively.The preliminary qPCR study of related markers (VEGF, ET-1, vWF) and Western bolting analysis of GP130 and p-STAT3 indicated a successful HUVECs injury in vitro DKD model, and the significant increasingly expression of Vegfa, ET-1, vWF mRNA in db/db mice was observed. Most importantly, the expression of miR-223-3p was indeed significantly decreased in both high glucose stimulated HUVECs and db/db DKD mice. Of which, the target gene IL6ST also showed significantly high expression.

In conclusion, these results indicated that the expression change of miR-223-3p in vitro and vivo DKD model may related to endothelial cell injury with DKD progression.

Key words: Diabetic kidney disease (DKD) , miR-223-3p, HUVECs, db/db mice, IL6ST.


P.Tang: None. Z.Jingrong: None. L.Zhang: None.


National Natural Science Foundation of China (81960156) and Health Science and Technology Program of Yunnan Province[2019FE001 (-040) ]

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