TY - JOUR
T1 - Antibody-mediated endothelial cell damage via nitric oxide
AU - Lin, Y. S.
AU - Lin, C. F.
AU - Lei, H. Y.
AU - Liu, H. S.
AU - Yeh, T. M.
AU - Chen, S. H.
AU - Liu, C. C.
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
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U2 - 10.2174/1381612043453469
DO - 10.2174/1381612043453469
M3 - Review article
C2 - 14754400
AN - SCOPUS:0346025498
SN - 1381-6128
VL - 10
SP - 213
EP - 221
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
IS - 2
ER -
