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23 February 2017 : Laboratory Research  

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

Xiaozhong Huang1ABE, Hui Xie1CD*, Guanhua Xue1CDF, Meng Ye1DF, Lan Zhang1CF

DOI: 10.12659/MSM.899443

Med Sci Monit 2017; 23:975-983

Abstract

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.

Keywords: Diabetic Angiopathies

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Medical Science Monitor Basic Research eISSN: 2325-4416
Medical Science Monitor Basic Research eISSN: 2325-4416