Antibody-mediated endothelial cell damage via 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 anti-endothelial cell antibody (AECA) in some cases of autoimmune disease. However, the molecular mechanisms of AECA-mediated 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.

journal_name

Curr Pharm Des

authors

Lin YS,Lin CF,Lei HY,Liu HS,Yeh TM,Chen SH,Liu CC

doi

10.2174/1381612043453469

subject

Has Abstract

pub_date

2004-01-01 00:00:00

pages

213-21

issue

2

eissn

1381-6128

issn

1873-4286

journal_volume

10

pub_type

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