Lectin-Like Oxidized Low-Density Lipoprotein 1 Receptor in a Reduced Uteroplacental Perfusion Pressure Rat Model of Preeclampsia

Preeclampsia is a major cause of maternal and fetal morbidity and mortality that has been associated with endothelial dysfunction attributed, in part, to dyslipidemia, an imbalance in angiogenic factors and oxidative stress. One of the many factors that have been shown to be elevated in women with p...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2012-05, Vol.59 (5), p.1014-1020
Main Authors: Morton, Jude S, Abdalvand, Ali, Jiang, Yanyan, Sawamura, Tatsuya, Uwiera, Richard R.E, Davidge, Sandra T
Format: Article
Language:English
Subjects:
Animals
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Biomarkers - metabolism
Blood and lymphatic vessels
Cardiology. Vascular system
Endothelium, Vascular - pathology
Endothelium, Vascular - physiopathology
Experimental diseases
Female
Medical sciences
Models, Animal
Nitric Oxide Synthase Type III - metabolism
Perfusion - methods
Peroxynitrous Acid - metabolism
Placenta - blood supply
Placental Circulation - physiology
Pre-Eclampsia - metabolism
Pre-Eclampsia - physiopathology
Pregnancy
Pressure
Random Allocation
Rats
Reference Values
Scavenger Receptors, Class E - metabolism
Statistics, Nonparametric
Superoxides - metabolism
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Summary:Preeclampsia is a major cause of maternal and fetal morbidity and mortality that has been associated with endothelial dysfunction attributed, in part, to dyslipidemia, an imbalance in angiogenic factors and oxidative stress. One of the many factors that have been shown to be elevated in women with preeclampsia is low-density lipoprotein (LDL) and the more oxidizable, small dense LDL, which can lead to increased vascular oxidative stress and decreased bioavailability of NO. Lectin-like oxidized LDL-1 receptor (LOX-1) is a specific receptor for oxidized LDL. We hypothesized that a reduction of placental perfusion using a rat model of reduced uteroplacental perfusion pressure would result in enhanced LOX-1 expression in the maternal vasculature causing impaired vascular endothelial function through the actions of increased superoxide production and decreased NO-mediated vasodilation. We demonstrated a significant increase in the expression of the LOX-1 receptor (4.3-fold; P=0.002), endothelial NO synthase (2.7-fold; P=0.001), and superoxide (P=0.02) in thoracic aorta of the reduced uteroplacental perfusion pressure model, whereas maximal vasodilator function was modestly decreased (P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.112.191825