Long Non-Coding RNA, Small Nucleolar RNA Host Gene 5, Inhibits the Oxidized Low-Density Lipoprotein Induced Vascular Endothelial Cell Injury by Targeting miR-26a-5p

Abstract

Atherosclerosis is the major cause of cardiovascular disease, and endothelial cell injury is the primary atherogenic factor. Long non-coding RNAs (lncRNAs) are increasingly implicated as critical regulators of disease progression. Still, the role of lncRNA in endothelial cell injury is largely unknown. This issue was explored in control, ox-LDL stimulated, ox-LDL stimulated+transfected negative control vector, and ox-LDL stimulated+SNHG5 overexpression vector EA. hy926 cells. Quantitative real-time PCR used to assess the expression of SNHG5 and miR-26a-5p. Flow cytometry was used to evaluate cell apoptosis. Activity or concentration of SOD, MDA, CAT, and reactive oxygen species (ROS) was measured to assess oxidative stress. Western blotting was used to examine protein-level expression of cleaved Caspase-3, cleaved Caspase-9, and cyt-c in cytoplasm and mitochondria. Potential binding sites between SNHG5 and miR-26a-5p were predicted using Starbase software, and dual-luciferase reporter assays were used to identify target relationships. SNHG5 expression in cells following ox-LDL treatment was downregulated in EA. hy926 cells. Ox-LDL treatment promotes apoptosis, and increased C-Caspase-3, C-Caspase-9, and cytoplasmic cyt-c protein levels. MDA concentration and ROS activity were increased, while the activity of SOD and CAT was decreased. Transfection with SNHG5 reversed the effects of ox-LDL on cell apoptosis and oxidative stress. SNHG5 targeted miR-26a-5p and regulated its expression. miR-26a-5p mimics reversed SNHG5 modulation of apoptosis and oxidative stress. lncRNA SNHG5 targets to miR-26a-5p to regulate vascular endothelial cell injury induced by ox-LDL.