title: MiR-3202 - Promoted H5V Cell Apoptosis by Directly Targeting Fas Apoptotic Inhibitory Molecule 2 (FAIM2) in High Glucose Condition.
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.
authors.affiliation: Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland).
authors.forename: Xiaozhong
authors.initials: X
authors.lastname: Huang
authors.affiliation: Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland).
authors.forename: Hui
authors.initials: H
authors.lastname: Xie
authors.affiliation: Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland).
authors.forename: Guanhua
authors.initials: G
authors.lastname: Xue
authors.affiliation: Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland).
authors.forename: Meng
authors.initials: M
authors.lastname: Ye
authors.affiliation: Department of Vascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (mainland).
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002460:Cell Line; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D053200:Fas-Associated Death Domain Protein / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism; D006943:Hyperglycemia / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism*; D051379:Mice; D035683:MicroRNAs / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000378:metabolism*; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: C505534:Fadd protein, mouse; D053200:Fas-Associated Death Domain Protein; D008565:Membrane Proteins; D035683:MicroRNAs; D009419:Nerve Tissue Proteins; D019014:fas Receptor; C523971:lifeguard protein, mouse; D005947:Glucose