FAS and FAS-L expression by human endothelial cells from different body districts: Effects of TNF-α

E. Ciusani, M. Gelati, M. Girelli, E. A. Parati, A. Salmaggi

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Abstract

One of the functions of endothelial cells (EC) coating the luminal surface of the vessel wall is the control and regulation of inflammation in the tissues. This function is driven by differential expression of adhesion molecules and may be regulated by cytokines. Moreover, EC have been shown to exert a cytotoxic activity towards Fas+ infiltrating lymphocytes due to the constitutive expression of Fas-ligand. On the other hand, the EC themselves express Fas, although they are normally resistant to Fas-ligand-induced apoptosis. Since apoptosis of EC may also be a crucial event in the development of inflammation, in the present study the effect of TNF-α stimulation on Fas and Fas-ligand expression on human EC has been investigated. EC from different areas (adult umbilical vein, aorta, heart and brain microvessels and embryonal heart microvessels) were cultured in vitro by standard techniques. At confluence, cells were either stimulated with TNF α (50 ng/ml) or not for 24 h. Cells were then recovered and stained with anti CD31, anti Fas and anti Fas-ligand and analysed using flow cytometry. Constitutive expression of Fas and Fas-ligand was detected in all EC analysed with no differences among the various districts. A significant increase in the expression of Fas was detected after TNF α stimulation while - under our experimental conditions - no regulation was detected in Fas-ligand expression. To assess whether the TNF-induced increase in Fas expression was associated with an increased susceptibility to Fas-dependent apoptosis, EC were cultured in the presence of an anti-Fas antibody able to induce apoptosis. Preliminary results on embryonal heart EC showed that treatment with TNF was not able to increase the susceptibility of these cells to Fas-dependent apoptosis.

Original languageEnglish
JournalNeurological Sciences
Volume21
Issue number4 SUPPL.
Publication statusPublished - 2000

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ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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