Downregulation of miR-210-3p Attenuates High Glucose-Induced Angiogenesis of Vascular Endothelial Cells via Targeting FGFRL1

Abstract

Introduction: Vascular endothelial cell injury and angiogenesis induced by hyperglycemia are the main pathological basis of vascular complications in diabetes mellitus. The purpose of our study was to investigate the role and mechanism of miR-210-3p on high glucose-induced angiogenesis. Methods: Human umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG) to mimic the pathological process of hyperglycemia. HUVECs were divided into the Control group, HG group, HG+inhibitor-NC group, and HG+miR-210-3p inhibitor group. Proliferation and migration were tested by wound healing assay, tube formation, and Transwell assay. Quantitation real-time PCR and Western blots were performed to determine the expression of miR-210-3p and relative proteins, respectively. Results: The level of miR-210-3p significantly increased in HUVECs treated by HG. The knockdown of miR-210-3p attenuated the tube formation, proliferation, and migration of cultured HUVECs in vitro to inhibit angiogenesis by increasing the expression of fibroblast growth factor receptor-like 1 (FGFRL1) and then attenuating the phosphorylation of STAT3, ERK, and ATK. Conclusion: Our study revealed that miR-210-3p might be a promising target for the treatment of diabetic-associated vascular injury.