Mechanism of miR-30a-5p in Human Microvascular Endothelial Injury Induced by High Glucose

BAI Youju^1,2, ZHANG Lu^1,2, ZHANG Jiao1,2, ZHOU Bo¹*

(¹Department of Endocrinology, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China; ²The Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China)

Abstract:

This study was to investigate the effect of miR-30a-5p on the biological behavior of human microvascular endothelial cells cultured in high glucose and its possible underlying mechanism. RT-qPCR was used to detect the expression of miR-30a-5p in the normal glucose group, osmotic pressure group and high glucose group respectively. Meanwhile, the cell proliferation, migration, tube formation and senescence were observed with or without up-regulated miR-30a-5p through EdU staining, Transwell assay, tube formation assay, β-galactosidase staining and the expression of p21 analysis. Finally, the expression of p53 in each group was detected to explore whether the protective effect of miR-30a-5p on human microvascular endothelial cells under high glucose conditions is to directly target p53. Result shows that high glucose can significantly down-regulate the expression of miR-30a-5p in endothelial cells, promoting cell senescence, and inhibit its proliferation, migration and tube formation. Up-regulation of miR-30a-5p can reduce the cell senescence induced by high glucose, and reverse the inhibitory effect of high glucose on its biological behavior to a certain extent. In addition, the study also found that although high glucose significantly reduced the expression of miR-30a-5p and increased the expression of p53, there was no parallel change in p53 expression after upregulation of miR-30a-5p. That suggests that miR-30a-5p may improve the biological behavior of endothelial cells under high glucose through other mechanism, rather than directly targeting p53.