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Uncoupling protein-2 protects endothelial function in diet-induced obese mice
Tian X.Y.3; Wong W.T.3; Xu A.2; Lu Y.3; Zhang Y.3; Wang L.3; Cheang W.S.3; Wang Y.2; Yao X.3; Huang Y.3
2012-04-27
Source PublicationCirculation Research
ISSN00097330 15244571
Volume110Issue:9Pages:1211-1216
Abstract

Rationale: Previous studies indicate uncoupling protein-2 (UCP2) as an antioxidant defense against endothelial dysfunction in hypertension. UCP2 also regulates insulin secretion and action. However, the role of UCP2 in endothelial dysfunction associated with diabetes and obesity is unclear. Objective: UCP2 protects against endothelial dysfunction induced by high-fat diet through inhibition of reactive oxygen species (ROS) production, and subsequent increase of nitric oxide bioavailability. Methods and Results: Endothelium-dependent relaxation (EDR) in aortae and mesenteric arteries in response to acetylcholine was measured in wire myograph. Flow-mediated vasodilatation in 2-order mesenteric arteries was measured in pressure myograph. ROS production is measured by CM-H2DCFDA and DHE fluorescence. High-glucose exposure reduced EDR in mouse aortae, which was exaggerated in UCP2 knockout (KO) mice, whereas UCP2 overexpression by adenoviral infection (AdUCP2) restored the impaired EDR. Impairment of EDR and flow-mediated vasodilatation in aortae and mesenteric arteries from high-fat diet-induced obese mice (DIO) was exaggerated in UCP2KO DIO mice compared with wild-type DIO littermates, whereas AdUCP2 i.v. injection restored both EDR and flow-mediated vasodilatation in DIO mice. Improved EDR in mesenteric arteries was inhibited by nitric oxide synthase inhibitor. UCP2 overexpression also inhibited intracellular ROS production in the en face endothelium of aorta and mesenteric artery of DIO mice, whereas UCP2 deficiency enhanced ROS production. Conclusions: UCP2 preserves endothelial function through increasing nitric oxide bioavailability secondary to the inhibition of ROS production in the endothelium of obese diabetic mice. © 2012 American Heart Association, Inc.

KeywordDiabetes Endothelial Dysfunction Oxidative Stress Uncoupling Protein Vasodilatation
DOI10.1161/CIRCRESAHA.111.262170
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaCardiovascular System & Cardiology ; Hematology
WOS SubjectCardiac & Cardiovascular Systems ; Hematology ; Peripheral Vascular Disease
WOS IDWOS:000303406200016
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Cited Times [WOS]:97   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Affiliation1.New Laboratory Block
2.The University of Hong Kong
3.Chinese University of Hong Kong
Recommended Citation
GB/T 7714
Tian X.Y.,Wong W.T.,Xu A.,et al. Uncoupling protein-2 protects endothelial function in diet-induced obese mice[J]. Circulation Research,2012,110(9):1211-1216.
APA Tian X.Y.,Wong W.T.,Xu A.,Lu Y.,Zhang Y.,Wang L.,Cheang W.S.,Wang Y.,Yao X.,&Huang Y..(2012).Uncoupling protein-2 protects endothelial function in diet-induced obese mice.Circulation Research,110(9),1211-1216.
MLA Tian X.Y.,et al."Uncoupling protein-2 protects endothelial function in diet-induced obese mice".Circulation Research 110.9(2012):1211-1216.
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