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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
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Adenovirus-mediated overexpression of c-Jun and c-Fos induces intercellular adhesion molecule-1 and monocyte

N Wang1, L Verna, S Hardy

  • 1Division of Biomedical Sciences, University of California, Riverside 92521, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|September 10, 1999
PubMed

Insights

Activator protein-1 (AP-1) overexpression in endothelial cells induces intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) gene expression. This AP-1 activation may contribute to vascular inflammation and disease.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Activator protein-1 (AP-1), c-Jun, and c-Fos are key regulators of cellular processes.
  • AP-1 acts as a distal target and mediator in signal transduction pathways.
  • Gene regulation by AP-1 influences cell function, proliferation, and differentiation.

Purpose of the Study:

  • To investigate the role of AP-1 in regulating gene expression in human vascular endothelial cells (ECs).
  • To determine if AP-1 directly influences the expression of adhesion molecules and chemokines.
  • To explore the potential involvement of AP-1 in vascular disorders.

Main Methods:

  • Adenovirus-mediated gene transfer was employed to overexpress AP-1 proteins in ECs.
  • Gene expression levels of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) were analyzed.
  • The mechanism of AP-1-induced gene expression was assessed for independence from nuclear factor-kappaB (NF-κB).

Main Results:

  • Overexpression of AP-1 proteins led to the coinduction of ICAM-1 and MCP-1 gene expression in human ECs.
  • The observed AP-1-induced gene expression was independent of NF-κB signaling.
  • Induced ICAM-1 and MCP-1 expression in ECs is linked to endothelial activation and vascular pathologies.

Conclusions:

  • AP-1 activation directly upregulates ICAM-1 and MCP-1 in vascular endothelial cells.
  • AP-1 plays a role in endothelial activation, potentially independent of NF-κB.
  • AP-1 activation is suggested to be significant in the pathogenesis of inflammation, angiogenesis, and atherogenesis.

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