Abstract
Vascular disorders, resulting from endothelial cell dysfunction, may be caused by various stimuli, including infectious pathogens, cytotoxic reagents, and pathophysiological mechanisms mediated by immune responses. Endothelial cell dysfunction characterized by apoptosis and abnormal immune activation is, at least in part, induced by antiendothelial cell antibody (AECA) in some cases of autoimmune disease. However, the molecular mechanisms of AECAmediated pathogenetic damage to host vascular system remain unclear. The dual role of nitric oxide (NO) both in endothelial cell apoptosis and survival has been described. In this paper, endothelial cell apoptosis caused by the presence of cross-reactive AECA via a NO-mediated mechanism is demonstrated in dengue virus infection. Endothelial cells undergo apoptosis via the mitochondria-dependent pathway that is regulated by NO production. NO-regulated endothelial cell injury thus may play a role in the disruption of vessel endothelium and contribute to the AECA-induced pathogenesis of vasculopathy. The modulation of NO may provide the therapeutic strategies for autoimmune diseases by preventing the AECA-mediated endothelial cell damage.
Keywords: anti-endothelial cell antibody, apoptosis, nitric oxide
Current Pharmaceutical Design
Title: Antibody-Mediated Endothelial Cell Damage Via Nitric Oxide
Volume: 10 Issue: 2
Author(s): Y. S. Lin, C. F. Lin, H. Y. Lei, H. S. Liu, T. M. Yeh, S. H. Chen and C. C. Liu
Affiliation:
Keywords: anti-endothelial cell antibody, apoptosis, nitric oxide
Abstract: Vascular disorders, resulting from endothelial cell dysfunction, may be caused by various stimuli, including infectious pathogens, cytotoxic reagents, and pathophysiological mechanisms mediated by immune responses. Endothelial cell dysfunction characterized by apoptosis and abnormal immune activation is, at least in part, induced by antiendothelial cell antibody (AECA) in some cases of autoimmune disease. However, the molecular mechanisms of AECAmediated pathogenetic damage to host vascular system remain unclear. The dual role of nitric oxide (NO) both in endothelial cell apoptosis and survival has been described. In this paper, endothelial cell apoptosis caused by the presence of cross-reactive AECA via a NO-mediated mechanism is demonstrated in dengue virus infection. Endothelial cells undergo apoptosis via the mitochondria-dependent pathway that is regulated by NO production. NO-regulated endothelial cell injury thus may play a role in the disruption of vessel endothelium and contribute to the AECA-induced pathogenesis of vasculopathy. The modulation of NO may provide the therapeutic strategies for autoimmune diseases by preventing the AECA-mediated endothelial cell damage.
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Cite this article as:
Lin S. Y., Lin F. C., Lei Y. H., Liu S. H., Yeh M. T., Chen H. S. and Liu C. C., Antibody-Mediated Endothelial Cell Damage Via Nitric Oxide, Current Pharmaceutical Design 2004; 10 (2) . https://dx.doi.org/10.2174/1381612043453469
DOI https://dx.doi.org/10.2174/1381612043453469 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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