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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Antibody-Mediated Endothelial Cell Damage Via Nitric Oxide

Author(s): Y. S. Lin, C. F. Lin, H. Y. Lei, H. S. Liu, T. M. Yeh, S. H. Chen and C. C. Liu

Volume 10, Issue 2, 2004

Page: [213 - 221] Pages: 9

DOI: 10.2174/1381612043453469

Price: $65

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


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