miR‑214 mediates vascular inflammation and apoptosis via PTEN expression

Mol Med Rep. 2018 Aug;18(2):2229-2236. doi: 10.3892/mmr.2018.9185. Epub 2018 Jun 18.

Abstract

The present study aimed to investigate the role of miR‑214 on inflammation and apoptosis in the vascular system and to examine its potential mechanisms. Anti‑miR‑214 mimics were used to downregulate miR‑214 expression in HUVECs. Cell viability and the apoptosis rate were measured using MTT assay and flow cytometry. Tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels were measured using ELISA kits. Following this, caspase‑3/9, Bax, phosphatase and tensin homolog (PTEN), nuclear factor (NF)‑κB and phosphorylated‑(p)‑protein kinase B (Akt) protein expression were analyzed using western blotting. The results demonstrated that anti‑miR‑214 mimics inhibited cell proliferation, increased apoptosis and inflammatory factors (TNF‑α, IL‑1β, IL‑6 and IL‑18 levels), inhibited cell proliferation, and induced Bax protein expression in TNF‑α‑induced vascular endothelial cells through induction of PTEN and NF‑κB protein expression and inhibition of Akt protein expression. The PTEN inhibitor inhibited the function of anti‑miR‑214 on apoptosis and inflammation in TNF‑α‑induced inflammation vascular endothelial cells through the PTEN/Akt signaling pathway. These results suggest that miR‑214 mediates vascular inflammation and apoptosis via PTEN expression.

MeSH terms

  • Apoptosis Regulatory Proteins / metabolism
  • Apoptosis*
  • Cytokines / metabolism
  • Gene Expression Regulation, Enzymologic*
  • Human Umbilical Vein Endothelial Cells / metabolism*
  • Human Umbilical Vein Endothelial Cells / pathology
  • Humans
  • Inflammation / metabolism
  • Inflammation / pathology
  • MicroRNAs / metabolism*
  • PTEN Phosphohydrolase / biosynthesis*
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction*
  • Vasculitis / metabolism*
  • Vasculitis / pathology

Substances

  • Apoptosis Regulatory Proteins
  • Cytokines
  • MIRN214 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human