MiR-92a regulates viability and angiogenesis of endothelial cells under oxidative stress

Lan Zhang, Mi Zhou, Gangjian Qin, Neal L. Weintraub, Yaoliang Tang

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

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 (H 2O2) was used to induce oxidative stress in human umbilical vein endothelial cells (HUVEC). Pre-miR-92a treatment decreased H 2O2-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.

Original languageEnglish (US)
Pages (from-to)952-958
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume446
Issue number4
DOIs
StatePublished - Apr 18 2014

Keywords

  • Angiogenesis
  • Apoptosis
  • Oxidative stress
  • microRNA

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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