Fas ligation triggers apoptosis in macrophages but not endothelial cells

Richardson, Bruce C.; Lalwani, Narendra D.; Johnson, Kent J.; Marks, Rebecca A.

doi:10.1002/eji.1830241111

Cited by 182 publications

(143 citation statements)

References 30 publications

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“…Addition of antioxidants (vitamins C and E) completely prevents the activation of caspase-3 by oxLDL and inhibits the apoptotic process (Dimmeler et al, 1997a). Although vascular endothelial cells are normally resistant to Fasmediated cell apoptosis (Richardson et al, 1994), apoptosis induced by OxLDL in cultured endothelial cells and endothelium of arterial explants appears to be inhibited by Fas ligand neutralizing antibodies, suggesting that OxLDL may promote Fas-mediated endothelial cell apoptosis .…”

Section: Induction Of Pro-apoptotic Pathwaysmentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

307

214

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Apoptotic death has now been recognized in a number of common and threatening vascular diseases, including atherosclerosis. Interest in apoptosis research relates to the fact that apoptosis, in contrast to oncosis, is a highly regulated process of cell death which raises the hope for the development of speci®c therapeutic strategies to alter disease progression. This review summarizes the mechanisms involved in vascular endothelial and smooth muscle cell survival/apoptosis, and the potential roles of apoptotic death in atherosclerosis and restenosis. The potential e ects of modulation of apoptosis in these diseases are also discussed.

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Section: Induction Of Pro-apoptotic Pathwaysmentioning

confidence: 99%

Apoptosis in the vasculature: mechanisms and functional importance

Mallat¹,

Tedgui²

2000

British J Pharmacology

307

214

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show abstract

“…In contrast to many cell types, vascular endothelial cells are normally resistant to Fas-mediated apoptosis (23)(24)(25)(26). Although endothelial cells express an intact Fas pathway, death signals appear to be blocked by the coexpression of inhibitory molecules (27,28).…”

Section: Fas Ligand Overexpression On Allograft Endothelium Inhibitsmentioning

confidence: 99%

Fas Ligand Overexpression on Allograft Endothelium Inhibits Inflammatory Cell Infiltration and Transplant-Associated Intimal Hyperplasia

Sata

Luo

Walsh

2001

The Journal of Immunology

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Despite recent advances in immunosuppressive therapy, accelerated coronary atherosclerosis remains a major problem in the long-term survival of transplant recipients. Chronic graft vasculopathy is believed to result from recipient inflammatory responses, and it is characterized by early mononuclear cell infiltration of the transplanted vessel. Here we show that endothelial cells can be genetically modified to overexpress functional, cell-surface Fas ligand (FasL) by adenovirus-mediated gene transfer without undergoing self-destruction. In a rodent model of transplant graft vasculopathy, endothelial overexpression of FasL attenuated T cell and macrophage infiltration at 1 wk posttransplantation. These vessels also displayed reduced neointima formation at one and 2 mo posttransplantation. These results indicate that inhibition of the early inflammatory response to allografted vessels by endothelial cell-specific overexpression of FasL may have utility in the treatment of transplant arteriosclerosis.

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“…1b). Since it has been reported that IFN-␥ increases Fas expression in some cell types (8,40,41), we examined the effect of this cytokine alone and in combination with TNF-␣ on Sertoli cell Fas expression by Western blotting analysis. As shown in Fig.…”

Section: Fas Ag Is Present In Cultured Mouse Sertoli Cells and Its Exmentioning

confidence: 99%

TNF-α and IFN-γ Regulate Expression and Function of the Fas System in the Seminiferous Epithelium

Riccioli

Starace

D’Alessio

et al. 2000

The Journal of Immunology

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Sertoli cells have long been considered to be involved in the regulation of the immune response in the testis. More recently, the Fas system has been implicated in the maintenance of the immune privilege in the testis as well as in the regulation of germ cell apoptosis. However, the control of Fas and Fas ligand (FasL) expression in the testis remains unknown. In the present study, we demonstrate that cultured mouse Sertoli cells constitutively express a low level of membrane-bound Fas protein, but not a soluble form of Fas. Sertoli cells stimulated with TNF-α and IFN-γ markedly increase the expression of both soluble and membrane-bound Fas in a dose-dependent manner. The up-regulated membrane-bound Fas protein is functionally active because it induces a significant level of Sertoli cell death in the presence of Neuro-2a FasL+ effector cells. Interestingly, the soluble form of Fas, which is induced by the same cytokines but has an antiapoptotic effect, is also functional. In fact, conditioned media from TNF-α-stimulated Sertoli cell cultures inhibit Neuro-2a FasL+-induced cell death. Taken together, our data suggest a possible regulatory role of TNF-α and IFN-γ on Fas-mediated apoptosis in the testis through disruption of the balance between different forms of Fas.

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Fas ligation triggers apoptosis in macrophages but not endothelial cells

Cited by 182 publications

References 30 publications

Apoptosis in the vasculature: mechanisms and functional importance

Apoptosis in the vasculature: mechanisms and functional importance

Fas Ligand Overexpression on Allograft Endothelium Inhibits Inflammatory Cell Infiltration and Transplant-Associated Intimal Hyperplasia

TNF-α and IFN-γ Regulate Expression and Function of the Fas System in the Seminiferous Epithelium

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