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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2078-2084.)
© 1999 American Heart Association, Inc.

Vascular Biology

Adenovirus-Mediated Overexpression of c-Jun and c-Fos Induces Intercellular Adhesion Molecule-1 and Monocyte Chemoattractant Protein-1 in Human Endothelial Cells

Nanping Wang; Lynne Verna; Stephen Hardy; John Forsayeth; Yi Zhu; Michael B. Stemerman

From the Division of Biomedical Sciences (N.W., L.V., Y.Z., M.B.S.), University of California, Riverside; Chiron Corp (S.H.), Emerville; and Elan Pharmaceuticals (J.F.), Menlo Park, Calif.

Correspondence to M.B. Stemerman, MD, Division of Biomedical Sciences, University of California, Riverside, CA 92521. E-mail michael.stemerman{at}ucr.edu

Abstract—As distal targets and mediators of signal transduction pathways, activator protein-1 (AP-1), c-Jun, and c-Fos are among the primary regulators of genes involved in cell function, proliferation, and differentiation. By using adenovirus-mediated gene transfer, we show that overexpression of AP-1 proteins directly causes coinduction of gene expression of an adhesion molecule, intercellular adhesion molecule-1 (ICAM-1), and a chemokine, monocyte chemoattractant protein-1 (MCP-1), in human vascular endothelial cells (ECs). The AP-1–induced gene expression occurs through a mechanism independent of nuclear factor-B. Because the induced expression of ICAM-1 and MCP-1 in ECs has been implicated in endothelial activation and a number of important vascular disorders, it is suggested that AP-1 activation may play an important role in the pathogeneses of inflammation, angiogenesis, and atherogenesis.

Key Words: endothelial activation • AP-1 • adenovirus • adhesion molecules • chemokines

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