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Updated: Jun 5, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
09:04

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

Oncostatin M-enhanced vascular endothelial growth factor expression in human vascular smooth muscle cells involves

Svitlana Demyanets1, Christoph Kaun, Kathrin Rychli

  • 1Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Basic Research in Cardiology
|December 22, 2010
PubMed

Insights

Oncostatin M (OSM) stimulates vascular endothelial growth factor (VEGF) production in human smooth muscle cells, potentially driving cardiovascular disease plaque growth. Interferon-gamma (IFN-γ) can reduce this OSM-induced VEGF production.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Cell Biology

Background:

  • Oncostatin M (OSM), a glycoprotein (gp)130 ligand, is implicated in inflammation and cardiovascular disease.
  • Inflammation and pathological angiogenesis are key processes in cardiovascular disease development.
  • Vascular smooth muscle cells (SMC) play a critical role in the pathogenesis of cardiovascular conditions.

Purpose of the Study:

  • To investigate the effect of OSM and other gp130 ligands on vascular endothelial growth factor (VEGF) production in human vascular SMC.
  • To explore the signaling pathways involved in OSM-induced VEGF production.
  • To analyze the expression of OSM and VEGF in human atherosclerotic lesions.

Main Methods:

  • Human coronary artery SMC (HCASMC) and human aortic SMC (HASMC) were treated with gp130 ligands.
  • VEGF protein levels were measured by ELISA; mRNA expression was analyzed by RT-PCR.
  • Western blotting was used to assess STAT1, STAT3, Akt, and p38 MAPK activation; inhibitors were employed to dissect signaling pathways.

Main Results:

  • OSM significantly increased VEGF production and upregulated VEGF and OSM receptor mRNA in HCASMC and HASMC.
  • Inhibitors of STAT3, p38 MAPK, Erk1/2, and PI3K pathways reduced OSM-induced VEGF synthesis.
  • OSM mRNA expression was detected in human atherosclerotic lesions, correlating positively with VEGF mRNA expression.

Conclusions:

  • OSM, present in atherosclerotic lesions, stimulates VEGF production by vascular SMC, suggesting a role in plaque angiogenesis and destabilization.
  • Interferon-gamma (IFN-γ) inhibited OSM-induced VEGF production in vascular SMC, indicating a potential counter-regulatory mechanism.
  • These findings highlight OSM as a potential therapeutic target in cardiovascular disease.

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