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https://hdl.handle.net/2440/11526
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Type: | Journal article |
Title: | TGT-β and endothelial cells inhibit VCAM-1 expression on human vascular smooth muscle cells |
Other Titles: | TGT-beta and endothelial cells inhibit VCAM-1 expression on human vascular smooth muscle cells |
Author: | Gamble, Jennifer R. Bradley, Sandy Noack, Leanne Vadas, Mathew Alexander |
Citation: | Arteriosclerosis, Thrombosis and Vascular Biology, 1995; 15(7):949-955 |
Publisher: | American Heart Association |
Issue Date: | 1995 |
ISSN: | 1079-5642 |
Statement of Responsibility: | Jennifer R. Gamble, Sandy Bradley, Leanne Noack, and Mathew A. Vadas |
Abstract: | Vascular smooth muscle cells (VSMCs) are normally devoid of the adhesion protein vascular cell adhesion molecule–1 (VCAM-1), which has, however, been observed on human VSMCs in atheroma. We now show that cultured human saphenous vein VSMCs express small amounts of VCAM-1 and that the cytokine tumor necrosis factor–α (TNF-α) induces, in a time- and dose-dependent fashion, a significant increase in its expression. Interleukin (IL)-4, IL-1, and to a lesser extent interferon gamma have similar effects. TNF-α–stimulated human VSMCs demonstrate increased binding of T lymphocytes that is totally VCAM-1 mediated. The cytokine transforming growth factor–β (TGF-β) at 2.0 ng/mL inhibited basal VCAM-1 expression by 84±8% and the induction by TNF-α by between 56±16% and 77±15% depending on the dose of TNF. Furthermore, coculture on opposing sides of a polycarbonate filter of human VSMCs with human umbilical vein endothelial cells also inhibited the induction of VCAM-1 by 47±6%. As active TGF-β is produced upon the coculture of VSMCs and endothelial cells, we suggest that the close physical proximity of these cells in vivo is responsible for the lack of expression of VCAM-1 on VSMCs and that the interruption of this contact in atheroma is an important pathogenic event. As VCAM-1 not only serves as an adhesion molecule but also as a costimulator of immune cells, its expression may be crucial in the propagation of vascular lesions. |
Keywords: | Atherogenesis; T cell adhesion; tumor necrosis factor; interleukin-4 |
DOI: | 10.1161/01.ATV.15.7.949 |
Appears in Collections: | Microbiology and Immunology publications |
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