title: MiR-92a regulates viability and angiogenesis of endothelial cells under oxidative stress.
abstract: Oxidative stress contributes to endothelial cell (EC) dysfunction, which is prevalent in ageing and atherosclerosis. MicroRNAs (miRs) are small, non-coding RNAs that post-transcriptionally regulate gene expression and play a key role in fine-tuning EC functional responses, including apoptosis and angiogenesis. MiR-92a is highly expressed in young endothelial cells in comparison with senescent endothelial cells, which exhibit increased oxidative stress and apoptosis. However, the impact of miR-92a treatment on EC viability and angiogenesis under oxidative stress is unknown. Hydrogen peroxide (H2O2) was used to induce oxidative stress in human umbilical vein endothelial cells (HUVEC). Pre-miR-92a treatment decreased H2O2-induced apoptosis of HUVEC as determined by TUNEL assay. Pre-miR-92a treatment enhanced capillary tube formation by HUVEC under oxidative stress, which was blocked by LY294002, an inhibitor of Akt phosphorylation. Interestingly, we also observed that inhibition of miR-92a by anti-miR-92a antisense can also enhance angiogenesis in HUVEC with and without oxidative stress exposure. Our results show that perturbation of miR-92a levels outside of its narrow "homeostatic" range may trigger endothelial cell angiogenesis, suggesting that the role of miR-92a in regulating angiogenesis is controversial and may vary depending on the experimental model and method of regulating miR-92a.
authors.affiliation: Department of Vascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China; Vascular Biology Center, Department of Medicine, Medical College of Georgia/Georgia Regents University, 1459 Laney Walker Blvd, Augusta, GA 30912, USA.
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Cardiac Surgery, Rui Jin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200025, China.
authors.forename: Mi
authors.initials: M
authors.lastname: Zhou
authors.affiliation: Feinberg Cardiovascular Research Institute, Department of Medicine-Cardiology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
authors.forename: Gangjian
authors.initials: G
authors.lastname: Qin
authors.affiliation: Vascular Biology Center, Department of Medicine, Medical College of Georgia/Georgia Regents University, 1459 Laney Walker Blvd, Augusta, GA 30912, USA.
authors.forename: Neal L
authors.initials: NL
authors.lastname: Weintraub
authors.affiliation: Vascular Biology Center, Department of Medicine, Medical College of Georgia/Georgia Regents University, 1459 Laney Walker Blvd, Augusta, GA 30912, USA. Electronic address: yaotang@gru.edu.
authors.forename: Yaoliang
authors.initials: Y
authors.lastname: Tang
mesh_terms: D002470:Cell Survival; D015536:Down-Regulation; D042783:Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D018919:Neovascularization, Physiologic; D018384:Oxidative Stress; D051059:PTEN Phosphohydrolase / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015854:Up-Regulation
chemical_list: C532045:MIRN29a microRNA, human; D035683:MicroRNAs; D006861:Hydrogen Peroxide; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase
keywords: Angiogenesis; Apoptosis; Oxidative stress; microRNA