MicroRNA-150 targets ELK1 and modulates the apoptosis induced by ox-LDL in endothelial cells

Mol Cell Biochem. 2017 May;429(1-2):45-58. doi: 10.1007/s11010-016-2935-3. Epub 2017 Jan 21.

Abstract

Atherosclerosis, a chronic inflammatory disease, is the major cause of life-threatening complications such as myocardial infarction and stroke. Endothelial cells (ECs) apoptosis plays a vital role in the initiation and progression of atherosclerosis. Although a subset of microRNAs (miRNAs) have been identified as critical regulators of atherosclerosis, studies on their participation in endothelial apoptosis in atherosclerosis have been limited. In the current study, we show that miRNA-150 (miR-150) expression was substantially up-regulated during the oxidized low-density lipoprotein (ox-LDL)-induced apoptosis in human umbilical cord vein endothelial cells (HUVECs). Forced expression of miR-150 enhanced apoptosis in ECs, whereas inhibition of miR-150 could partly alleviate apoptotic cell death mediated by ox-LDL. Further analysis identified ELK1 as a direct target of miR-150, and ELK1 knockdown abolished the anti-apoptotic effect of miR-150 inhibitor. These findings reveal a novel role of miR-150 in endothelial apoptosis and indicate a therapeutic potential of miR-150 for endothelial dysfunction and atherosclerosis.

Keywords: Apoptosis; Atherosclerosis; ELK1; HUVECs; MicroRNA-150.

MeSH terms

  • 3' Untranslated Regions
  • Apoptosis
  • Endothelial Cells / cytology*
  • Endothelial Cells / drug effects
  • Gene Expression Regulation
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Lipoproteins, LDL / pharmacology*
  • MicroRNAs / genetics*
  • ets-Domain Protein Elk-1 / genetics*

Substances

  • 3' Untranslated Regions
  • ELK1 protein, human
  • Lipoproteins, LDL
  • MIRN150 microRNA, human
  • MicroRNAs
  • ets-Domain Protein Elk-1
  • oxidized low density lipoprotein