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Cited by 197Atherosclerosis and Cardiovascular DiseasesCell death mechanisms and regulationNitric Oxide and Endothelin Effects

Tumor Necrosis Factor-α Promotes Macrophage-Induced Vascular Smooth Muscle Cell Apoptosis by Direct and Autocrine Mechanisms

Boyle, Joseph J., Weissberg, Peter L., Bennett, Martin R.·2003·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/01.atv.0000086961.44581.b7
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Abstract

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-α (TNF-α) 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-α. Two NO donors upregulated VSMC surface TNF-R1, and exogenous TNF-α induced VSMC apoptosis synergistically with the NO donor diethylenetriamine/NO, indicating that NO sensitizes VSMCs to TNF-α. Neutralizing anti–TNF-R1 antibodies inhibited macrophage activation assessed by Fas-L expression and NO secretion. Conclusions—TNF-α promotes macrophage-induced VSMC apoptosis by autocrine and direct pathways.

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Authors
Boyle, J. J., Weissberg, P. L., & Bennett, M. R.
Affiliations
Addenbrooke's Hospital (GB)
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-09
Volume
23
Issue
9
Pages
1553-1558
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/01.atv.0000086961.44581.b7
OpenAlex
W2131050523
Cited by
197
References
0
Citations by year
2026: 2 · 2025: 2 · 2024: 9 · 2023: 8 · 2022: 11 · 2021: 14 · 2020: 15 · 2019: 8 · 2018: 5 · 2017: 7 · 2016: 12 · 2015: 13 · 2014: 17 · 2013: 9 · 2012: 13
FWCI
2.26
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • British Heart Foundation
  • Medical Research Council
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
TNF-α, vascular smooth muscle cell apoptosis, macrophages, TNF receptor 1, autocrine signaling, plaque rupture, atherosclerosis, Fas ligand, monocyte activation, macrophage activation
MeSH terms
Antigens, Surface, Arteriosclerosis, Carotid Arteries, Cell Line, Cells, Cultured, Humans, Lipoproteins, Macrophage Activation, Macrophages, Membrane Glycoproteins, Monocytes, Muscle, Smooth, Vascular, Nitric Oxide, Polyamines, Rupture, Spontaneous, Tumor Necrosis Factor-alpha, Signal Transduction, Antigens, CD, Up-Regulation, Apoptosis, Receptors, Tumor Necrosis Factor, fas Receptor, Antibodies, Blocking, Nitric Oxide Donors, Intracellular Space, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Fas Ligand Protein

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