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Cited by 118Cell death mechanisms and regulationAtherosclerosis and Cardiovascular DiseasesBlood Coagulation and Thrombosis Mechanisms

Vascular Endothelial Cells and Smooth Muscle Cells Differ in Expression of Fas and Fas Ligand and in Sensitivity to Fas Ligand–Induced Cell Death: Implications for Vascular Disease and Therapy

Sata, Masataka, Suhara, Toshimitsu, Walsh, Kenneth·2000·Arteriosclerosis Thrombosis and Vascular Biology
DOI 10.1161/01.atv.20.2.309
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Abstract

Fas ligand (FasL) is a death factor that induces apoptosis in cells bearing its receptor, Fas. Fas and FasL have been detected in the vessel wall, and it has been proposed that Fas-mediated apoptosis has a role in physiological and pathological cell turnover in the vasculature. Here, we evaluated the expression of Fas in the presence and absence of cytokines on both endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). We also examined the sensitivity of ECs and VSMCs to Fas-mediated apoptosis induced by exposure to multiple Fas agonists: soluble FasL, anti-Fas antibody, and membrane-bound FasL resulting from transduction with a replication-defective adenovirus expressing FasL (Adeno-FasL). Cell-surface FasL expression was detected on human ECs with the use of 4 anti-FasL antibodies, whereas cell-surface FasL expression was not detected on VSMCs. Unstimulated ECs expressed relatively low levels of Fas, but expression was upregulated after treatment with tumor necrosis factor-alpha (TNF-alpha) or interferon gamma (IFN-gamma). In contrast, VSMCs expressed relatively high levels of Fas, and treatment with TNF-alpha or IFN-gamma induced little or no upregulation under the conditions of these assays. ECs were resistant to death after exposure to soluble FasL or agonist anti-Fas antibody and also after infection with Adeno-FasL in the presence or absence of cytokine treatment. In contrast, VSMCs remained viable in the presence of soluble FasL or agonist anti-Fas antibody, but they underwent apoptosis after infection with Adeno-FasL. IFN-gamma enhanced Adeno-FasL-induced death of VSMCs, but TNF-alpha did not. These findings provide insights about the potential role of Fas-mediated apoptosis in the vessel wall and suggest strategies to treat proliferative vascular diseases by exploiting the differential sensitivity of ECs and VSMCs to FasL-induced cell death.

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  • FAS is known to be active in both astrocytes and endothelial cells.

    “For example, expression of FAS is lower in astrocytes relative to endothelial cells; however, FAS is known to be active in both astrocytes (29) and endothelial cells (30) .”

    From Single cell transcriptome profiling of the human alcohol-dependent brain (2020) · cites this paper as [30]

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Authors
Sata, M., Suhara, T., & Walsh, K.
Affiliations
Tufts University (US)
ORCID
Venue
Arteriosclerosis Thrombosis and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2000-02
Volume
20
Issue
2
Pages
309-316
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/01.atv.20.2.309
OpenAlex
W2088247886
Cited by
118
References
44
Citations by year
2026: 2 · 2025: 3 · 2023: 1 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 2
FWCI
4.83
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Aging (AG15052)
  • National Heart, Lung, and Blood Institute (R01HL050692, HL50692)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-40197, R01AR040197)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords
Fas, Fas ligand, apoptosis, vascular endothelial cells, vascular smooth muscle cells, TNF-α, interferon-gamma, cytokine-induced gene expression
MeSH terms
Cell Survival, Cells, Cultured, Endothelium, Vascular, Gene Expression Regulation, Humans, Membrane Glycoproteins, Muscle, Smooth, Vascular, Vascular Diseases, Apoptosis, fas Receptor, Fas Ligand Protein

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