Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 8; Issue 3; 27 January 2006 Abstract
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Role of oxidative stress in the mediation of endothelial cell dysfunction in preeclampsia

Sowndramalingam Sankaralingam, Ivan A. Arenas, Manoj M. Lalu and Sandra T. Davidge

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Figure 1. Role of oxidative stress in the mediation of endothelial cell dysfunction in preeclampsia. Oxidised low-density lipoprotein (oxLDL), angiotensin II (ANG II) and tumour necrosis factor a (TNF-a) bind to lectin-like oxidised LDL receptor (LOX-1), ANG II type I receptor (AT1R) and TNF-a receptor (TNFR), respectively, and generate superoxide anions (O₂^.–) through NAD(P)H oxidase. Superoxide anions scavenge nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) to generate peroxynitrite (ONOO^–). Peroxynitrite increases inducible NOS (iNOS) and intercellular cell adhesion molecule 1 (ICAM-1) expression, a marker of endothelial dysfunction, by activation of nuclear factor kB (NF-kB) and decreases prostacyclin (PGI₂) synthase, which ultimately results in inflammation and vasoconstriction. Peroxynitrite also activates matrix metalloproteinase 2 (MMP-2), which subsequently cleaves ‘big endothelin-1’ (Big ET-1) to yield a more potent vasoconstrictor ET-1[1–32].

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