© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Effects of cross-linking ICAM-1 on the surface of human vascular smooth muscle cells: induction of VCAM-1 but no proliferation
Transplant Immunology Group, Imperial College School of Medicine, National Heart and Lung Institute, Heart Science Centre, Harefield Hospital, Harefield, Middlesex UB9 6JH, United Kingdom
* Corresponding author. Tel.: +44-1895-828-575; fax: +44-1895-828-900 marlene.rose{at}harefield.nthames.nhs.uk
Objective: Intercellular adhesion molecule (ICAM)-1 is an immunoglobulin-like cell adhesion molecule expressed by several cell types, including proliferating vascular smooth muscle cells (VSMC). Cross-linking ICAM-1 on the surface of different cell types has previously been shown to cause an increase in cellular activation within the cytoplasm. Here, our objective was to examine events following ligation of ICAM-1 on the surface of human VSMC. Methods: VSMC were isolated by explant from human pulmonary arteries or aortic tissue from cardiac transplant donors. ICAM-1 was ligated with monoclonal antibodies, followed by cross-linking with a secondary antibody. Activation of signalling pathways, proliferation and expression of a second adhesion molecule, vascular cell adhesion molecule (VCAM)-1 were investigated. Results: ICAM-1 cross-linking caused an increase in activation of extracellular regulated kinase (Erk)-1/-2 and Jun N-terminal kinase (JNK)-1/-2. mRNA and protein for VCAM-1 was observed after ICAM-1 cross-linking, and this was abrogated by addition of an upstream inhibitor of Erk-1/-2, PD98059. No increase in cell proliferation was observed. Conclusions: Ligation of ICAM-1 on the surface of vascular smooth muscle cells in vitro, leads to the expression of adhesion molecules associated with monocyte infiltration, but does not contribute to smooth muscle cell proliferation. In vivo, this might lead to prolongation of the inflammatory response within diseased blood vessels, by arresting monocytes within atherosclerotic plaques.
KEYWORDS Erk, extracellular regulated kinase; FGF, fibroblast growth factor; HUVEC, human umbilical vein endothelial cells; ICAM, intercellular adhesion molecule; JNK, Jun N-terminal kinase; LFA, leukocyte function-associated antigen; MAPK, mitogen activated protein kinase; MEK, MAPK/Erk kinase; MHC, major histocompatibility complex; PAGE, polyacrylamide gel electrophoresis; PDGF, platelet derived growth factor; PSI, proteasome inhibitor I; RAM, rabbit anti-mouse Ig; TCA, trichloroacetic acid; TGF, transforming growth factor; VCAM, vascular cell adhesion molecule; VLA, very late antigen; VSMC, vascular smooth muscle cells
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