on July 17, 2003
Published online before print July 17, 2003, doi: 10.1161/01.ATV.0000086961.44581.B7
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Submitted on April 11, 2003
Accepted on May 6, 2003
Tumor Necrosis Factor-
Promotes Macrophage-Induced Vascular Smooth Muscle Cell Apoptosis by Direct and Autocrine Mechanisms
Joseph J. Boyle *;
From the Unit of Cardiovascular Medicine, Addenbrooke's Hospital, Cambridge, UK.
* To whom correspondence should be addressed. E-mail: joseph.boyle{at}ic.ac.uk.
Objective--We have previously shown that human macrophages induce human plaque vascular smooth muscle cell (VSMC) apoptosis by cell-cell proximity, Fas-L, and nitric oxide (NO), thereby predisposing to plaque rupture. This study sought to analyze whether tumor necrosis factor-
(TNF-) contributes additionally to macrophage-induced VSMC apoptosis.
Methods and Results--Macrophage-induced VSMC apoptosis was examined in direct coculture. Antagonistic antibodies to TNF-receptor (R1) inhibited VSMC apoptosis, and preincubation of monocytes and VSMCs indicated that TNF-R1 on both cell types contributed to macrophage-induced VSMC apoptosis. Correspondingly, both monocytes and VSMCs expressed TNF-R1, and macrophages expressed cell surface TNF-. Two NO donors upregulated VSMC surface TNF-R1, and exogenous TNF- induced VSMC apoptosis synergistically with the NO donor diethylenetriamine/NO, indicating that NO sensitizes VSMCs to TNF-. Neutralizing anti-TNF-R1 antibodies inhibited macrophage activation assessed by Fas-L expression and NO secretion.
Conclusions--TNF- promotes macrophage-induced VSMC apoptosis by autocrine and direct pathways.
Key words: macrophages • atherosclerosis • plaque rupture • vascular smooth muscle cells • apoptosis • tumor necrosis factor
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