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MiR-3202 – Promoted H5V Cell Apoptosis by Directly Targeting Fas Apoptotic Inhibitory Molecule 2 (FAIM2) in High Glucose Condition

Xiaozhong Huang, Hui Xie, Guanhua Xue, Meng Ye, Lan Zhang

(Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland))

Med Sci Monit 2017; 23:975-983

DOI: 10.12659/MSM.899443

BACKGROUND: Vascular complications are a major concern for patients with diabetes. Endothelial cells (ECs) play a key role in vascular function. MicroRNAs (miRNAs) have been shown to play an important role in mediating EC function; miRNAs are vulnerable to hyperglycemic conditions. Previous reports verified that Fas apoptotic inhibitory molecule 2 (FAIM2) can inhibit cell apoptosis through repressing the FAS-associated death domain protein (FADD) pathway. This current study was designed to explore the potential involvement of miR-3202 in the pathogenesis of ECs in high-glucose conditions.
MATERIAL AND METHODS: The aim of this study was to investigate the role of miR-3202 in regulating hyperglycemia-induced ECs by targeting FAIM2. The endothelial cell line H5V was cultured in a high-glucose condition to induce damage to FAIM2 expression in ECs; mimic and inhibition of miR-3202 were used to enhance and depress miR-3202’s function to explore its function on FAIM2.
RESULTS: Our study showed that FAIM2 was inhibited by high-glucose conditions, and miRNA-3202 was induced by high-glucose conditions. FAIM2 was identified as the target gene of miRNA-3202; luciferase reporter assays confirmed that FAIM2 was downregulated by miR-3202 directly, that is, miR-3202 can upregulate Fas/FADD through inhibiting FAIM2.
CONCLUSIONS: MiR-3202 can promote EC apoptosis in hyperglycemic conditions, which demonstrated that EC apoptosis induced by high-glucose conditions partly depends on miR-3202 targeting FAIM2.

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