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The reciprocal relationship between adiponectin and LOX-1 in the regulation of endothelial dysfunction in ApoE knockout mice
Chen X.; Zhang H.; McAfee S.; Zhang C.
2010-09-01
Source PublicationAmerican Journal of Physiology - Heart and Circulatory Physiology
ISSN03636135 15221539
Volume299Issue:3
Abstract

We hypothesized that the reciprocal association between adiponectin and lectin-like oxidized LDL (ox-LDL) receptor (LOX)-1 contributes to the regulation of aortic endothelial dysfunction in atherosclerosis. To test this hypothesis, endothelium-dependent (ACh) and endothelium-independent (sodium nitroprusside) vasorelaxation of isolated aortic rings from control mice, apolipoprotein E (ApoE) knockout (KO) mice, and ApoE KO mice treated with either adiponectin (15 μg·day·mouse sc for 8 days) or neutralizing antibody to LOX-1 (anti-LOX-1, 16 μg/ml, 0.1 ml/mouse ip for 7 days) were examined. Although vasorelaxation to sodium nitroprusside was not different between control and ApoE KO mice, relaxation to ACh was impaired in ApoE KO mice. Adiponectin and anti-LOX-1 restored nitric oxide-mediated endothelium-dependent vasorelaxation in ApoE KO mice. Aortic ROS formation and ox-LDL uptake were increased in ApoE KO mice. Both adiponectin and anti-LOX-1 treatment reduced ROS production and aortic ox-LDL uptake. In mouse coronary artery endothelial cells, TNF-α incubation increased endothelial LOX-1 expression. Adiponectin reduced TNF-α-induced LOX-1 expression. Consistently, in ApoE KO mice, adiponectin treatment reversed elevated LOX-1 expression in aortas. Immunofluorescence staining showed that adiponectin was mainly colocalized with endothelial cells. Although adiponectin expression was lower in ApoE KO versus control mice, anti-LOX-1 increased aortic adiponectin expression, suggesting a reciprocal regulation between adiponectin and LOX-1. Moreover, both adiponectin and anti-LOX-1 reduced NF-κB expression in ApoE KO mice. Thus, adiponectin and LOX-1 may converge on NF-κB signaling to regulate their function. In conclusion, our results indicate that the reciprocal regulation between adiponectin and LOX-1 amplifies oxidative stress and ox-LDL uptake, leading to endothelial dysfunction in atherosclerosis. Copyright © 2010 the American Physiological Society.

KeywordAorta Apolipoprotein e Cytokine Lectin-like Oxidized Low-density Lipoprotein Receptor Oxidative Stress Vasorelaxation
DOI10.1152/ajpheart.01096.2009
URLView the original
Indexed BySCI
Language英语
WOS Research AreaCardiovascular System & Cardiology ; Physiology
WOS SubjectCardiac & Cardiovascular Systems ; Physiology ; Peripheral Vascular Disease
WOS IDWOS:000281537400005
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Cited Times [WOS]:28   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
AffiliationUniversity of Missouri-Columbia
Recommended Citation
GB/T 7714
Chen X.,Zhang H.,McAfee S.,et al. The reciprocal relationship between adiponectin and LOX-1 in the regulation of endothelial dysfunction in ApoE knockout mice[J]. American Journal of Physiology - Heart and Circulatory Physiology,2010,299(3).
APA Chen X.,Zhang H.,McAfee S.,&Zhang C..(2010).The reciprocal relationship between adiponectin and LOX-1 in the regulation of endothelial dysfunction in ApoE knockout mice.American Journal of Physiology - Heart and Circulatory Physiology,299(3).
MLA Chen X.,et al."The reciprocal relationship between adiponectin and LOX-1 in the regulation of endothelial dysfunction in ApoE knockout mice".American Journal of Physiology - Heart and Circulatory Physiology 299.3(2010).
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