FGF11 regulated by CTBP1-AS2/miR-520a-5p/miR-432-5p axis inhibits the progression and angiogenesis in high glucose-treated human microvascular endothelial cells.

INTRODUCTION

Type 2 diabetes mellitus (T2DM) is a common public health problem in the world. Patients with T2DM patients are accompanied with the risk of cardiovascular disease. Clarification of the potential molecular mechanism underlying vascular complications in diabetes mellitus (DM) is crucial for avoiding cardiovascular disease. Fibroblast growth factor 11 (FGF11) is a member of FGF family which, as reported before, can play a causative role in vascular dysfunction in T2DM.

MATERIALS &

METHODS

Human microvascular endothelial cells (HMVECs) were treated with high glucose (HG) to simulate T2DM model. Functional assays were carried out to disclose the cell proliferation, apoptosis, migration and angiogenesis of HG-treated HMVECs. Several mechanical experiments including RNA pull down, luciferase reporter and RNA immunoprecipitation (RIP) determined the regulatory mechanism of FGF11 in HG-treated HMVECs.

RESULTS

FGF11 displayed a low expression in HG-treated HMVECs. FGF11 overexpression inhibited proliferation, migration and angiogenesis of HMVECs while facilitated the cell apoptosis in under HG condition. Moreover, FGF11 was targeted by miR-520a-5p and miR-432-5p, and CTBP1-AS2 acted as a competing endogenous RNA to modulate FGF11 expression via sponging miR-520a-5p and miR-432-5p.

CONCLUSION

The axis of CTBP1-AS2/miR-520a-5p/miR-432-5p/FGF11 might be a potential target for T2DM treatment.