Interleukin-5 suppresses Vascular Endothelial Growth Factor-induced angiogenesis through STAT5 signaling

Cytokine. 2018 Oct:110:397-403. doi: 10.1016/j.cyto.2018.06.021. Epub 2018 Jun 18.

Abstract

Interleukin-5 (IL-5) is best known as key regulator in eosinophil-associated diseases such as asthma. While a connection to vascular changes in eosinophil-associated lung diseases is still elusive, recent evidence suggests that IL-5 may have an atheroprotective role. Here, we report an unexpected anti-angiogenic potential of IL-5 on vascular endothelial cells in vitro. IL-5 significantly inhibited fundamental functions of human lung microvascular endothelial cells (HMVEC-L) in vessel formation including VEGF-induced endothelial cell proliferation, migration and tube formation. Knockdown (KD) of STAT5 abolished the direct anti-angiogenic effect of IL-5 on VEGF-induced endothelial cell proliferation, migration and tube formation.

Keywords: Angiogenesis; Endothelial; Interleukin-5; STAT5; VEGF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / metabolism
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • Cells, Cultured
  • Endothelial Cells / metabolism
  • Endothelium, Vascular / metabolism
  • Humans
  • Interleukin-5 / metabolism*
  • Neovascularization, Pathologic / metabolism*
  • STAT5 Transcription Factor / metabolism*
  • Signal Transduction / physiology*
  • Tumor Suppressor Proteins / metabolism*
  • Vascular Endothelial Growth Factor A / metabolism*

Substances

  • Angiogenesis Inhibitors
  • IL5 protein, human
  • Interleukin-5
  • STAT5 Transcription Factor
  • STAT5A protein, human
  • Tumor Suppressor Proteins
  • Vascular Endothelial Growth Factor A