STAT6 mediates apoptosis of human coronary arterial endothelial cells by interleukin-13

Hypertens Res. 2008 Mar;31(3):535-41. doi: 10.1291/hypres.31.535.

Abstract

Interleukin (IL)-13 is a cytokine produced by type 2 helper T cells that has pathophysiological roles in allergic inflammation and fibrosis formation. IL-13 shares many functional properties with IL-4, which promotes apoptosis of endothelial cells (ECs). We here investigated the effects of IL-13 on apoptosis using human coronary artery endothelial cells (HCAECs). Assessment by WST-1 assay demonstrated that IL-13 as well as IL-4 significantly inhibited cell growth. IL-13 significantly attenuated the cell viability and induced apoptosis of HCAECs as well. Expression of mRNA for vascular endothelial cell growth factor, which maintains survival of ECs, was significantly diminished by IL-13. The effects of IL-13 and IL-4 were abolished by depletion of STAT6 using RNA interference. These results suggest that IL-13 attenuates EC viability by inducing apoptosis, and that STAT6 plays pivotal roles on IL-13- and IL-4-induced apoptosis in ECs.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Cell Proliferation
  • Cell Survival
  • Cells, Cultured
  • Coronary Vessels / cytology*
  • Coronary Vessels / metabolism*
  • Down-Regulation
  • Endothelial Cells / cytology*
  • Endothelial Cells / metabolism*
  • Humans
  • Interleukin-13 / physiology*
  • Interleukin-4 / physiology
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / metabolism
  • STAT6 Transcription Factor / metabolism*
  • Transfection
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Interleukin-13
  • RNA, Messenger
  • RNA, Small Interfering
  • STAT6 Transcription Factor
  • STAT6 protein, human
  • Vascular Endothelial Growth Factor A
  • Interleukin-4