Tumor Necrosis Factor‐o? Stimulates ICAM‐1 Expression in Human Vascular Smooth Muscle Cells
作者:
Thierry Couffinhal,
Cecile Duplaa,
Laurence Labat,
Jean-Marie Lamaziere,
Catherine Moreau,
Olga Printseva,
Jacques Bonnet,
期刊:
Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
(OVID Available online 1993)
卷期:
Volume 13,
issue 3
页码: 407-414
ISSN:1049-8834
年代: 1993
出版商: OVID
关键词: tumor necrosis factor-«;smooth muscle cells;intercellular adhesion molecule-1;adhesion monocytes;atherosclerosis
数据来源: OVID
摘要:
Human atherosclerotic plaques contain numerous smooth muscle cells (SMCs) that express intercellular adhesion molecule-1 (ICAM-1). Expression of ICAM-1 in different cells is known to be regulated by tumor necrosis factor-a (TNF-t*), which has recently been found to be present in the intimal thickening of human arteries. Therefore, we studied the effect of TNF-« on ICAM-1 mRNA content and surface expression in cultured human aortic SMCs by using the methods of Northern blotting and immunofluorescence flow cytometry. Under basal conditions of cultivation, ICAM-1 mRNA was not revealed in SMCs. However, treatment of the cells with recombinant human TNF-« induced substantial levels of ICAM-1 mRNA. The content of ICAM-1 on the surface of SMCs also increased in a doseand time-dependent manner after incubation with TNF-t*. Twenty-four hours of treatment with 10 ng/mL TNF-arled to an approximately 10-fold increase in ICAM-1 surface expression in the SMCs. Under the same conditions, pretreatment of SMCs with TNF-e* resulted in a twofold increase of their adhesiveness for monocytes. In the presence of anti-ICAM-1 monoclonal antibody 10F3, monocyte adhesion to TNF-«-pretreated SMCs was significantly inhibited, suggesting that the observed monocyte-SMC interaction involved the ICAM-1 expressed on SMC surfaces as a result of TNF-<x stimulation. These results led us to propose that TNF-« may act a regulator of functional ICAM-1 expression on the SMC surface and thus can increase the possibility of interactions between mononuclear cells and SMCs in atherosclerotic plaques.
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