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

摘要: 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 play a key role fine-tuning EC functional responses, including apoptosis angiogenesis. MiR-92a highly expressed young cells comparison with senescent cells, exhibit increased oxidative apoptosis. However, the impact of miR-92a treatment on viability angiogenesis under unknown. Hydrogen peroxide (H2O2) was used induce human umbilical vein (HUVEC). Pre-miR-92a decreased H2O2-induced HUVEC as determined by TUNEL assay. enhanced capillary tube formation stress, blocked LY294002, an inhibitor Akt phosphorylation. Interestingly, we also observed inhibition anti-miR-92a antisense can enhance without exposure. Our results show perturbation levels outside its narrow “homeostatic” range may trigger angiogenesis, suggesting regulating controversial vary depending experimental model method miR-92a.