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Conference Paper: Lipocalin-2, an inflammatory adipokine, uncouples endothelial nitric-oxide synthase and enhances endothelial dysfunction caused by dietary obesity

TitleLipocalin-2, an inflammatory adipokine, uncouples endothelial nitric-oxide synthase and enhances endothelial dysfunction caused by dietary obesity
Authors
KeywordsPharmacy and pharmacology environmental studies
Toxicology and environmental safety
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO
Citation
The 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 159-160 How to Cite?
AbstractEndothelial dysfunction contributes to the pathogenesis of cardiovascular diseases. Lipocalin-2 is a pro-inflammatory adipokine. Its circulating concentration positively associates with adiposity, dyslipidemia, hyperglycemia and insulin resistance. Lipocalin-2 deficiency protects mice from developing ageing- and obesity-induced insulin resistance. In the present study, endothelial function of wild type (WT) and lipocalin-2 knockout (Lcn2-KO) mice was compared by measuring isometric tensions in rings of aortae and carotid arteries from dietary obesity-challenged animals. High fat diet feeding for only three weeks significantly impaired endothelium-dependent relaxation (EDR) to insulin in aortae and enhanced endothelium-dependent contraction (EDC) to acetylcholine in carotid arteries. These endothelial dysfunctions were nearly abolished by lipocalin-2 deficiency. Insulin-induced Akt/eNOS phosphorylation was enhanced in aortae of Lcn2-KO mice. The increases in the ratio of eNOS monomers to dimers, and superoxide anion formation were significantly attenuated in mice without lipocalin-2. The level of nitrotyrosine in the total protein and precipitated eNOS of arteries from wide type mice was increased compared with that in Lcn2-KO vessels, despite a similar expression of eNOS protein. The basal and acetylcholine-stimulated superoxide anion production and COX-1 expression were diminished in Lcn2-KO arteries. Replacement with lipocalin-2 in Lcn2-KO mice time-dependently monomerized eNOS in the aorta, increased COX-1 expression levels, and impaired endothelial functions as demonstrated by reduced EDR and enhanced EDC. Lipocalin-2 plays a critical role in the development of obesity-induced endothelial dysfunction through modulation of eNOS activity and oxidative stress.
DescriptionFocused Conference Group: YI – Young Investigators’ Session. Paper No. 2293
Persistent Identifierhttp://hdl.handle.net/10722/126880
ISSN
2015 Impact Factor: 3.097
2015 SCImago Journal Rankings: 0.539

 

DC FieldValueLanguage
dc.contributor.authorLiu, JTCen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorMak, TWen_HK
dc.contributor.authorLiang, CFen_HK
dc.contributor.authorLaw, IKMen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2010-10-31T12:53:58Z-
dc.date.available2010-10-31T12:53:58Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 159-160en_HK
dc.identifier.issn1742-7835-
dc.identifier.urihttp://hdl.handle.net/10722/126880-
dc.descriptionFocused Conference Group: YI – Young Investigators’ Session. Paper No. 2293-
dc.description.abstractEndothelial dysfunction contributes to the pathogenesis of cardiovascular diseases. Lipocalin-2 is a pro-inflammatory adipokine. Its circulating concentration positively associates with adiposity, dyslipidemia, hyperglycemia and insulin resistance. Lipocalin-2 deficiency protects mice from developing ageing- and obesity-induced insulin resistance. In the present study, endothelial function of wild type (WT) and lipocalin-2 knockout (Lcn2-KO) mice was compared by measuring isometric tensions in rings of aortae and carotid arteries from dietary obesity-challenged animals. High fat diet feeding for only three weeks significantly impaired endothelium-dependent relaxation (EDR) to insulin in aortae and enhanced endothelium-dependent contraction (EDC) to acetylcholine in carotid arteries. These endothelial dysfunctions were nearly abolished by lipocalin-2 deficiency. Insulin-induced Akt/eNOS phosphorylation was enhanced in aortae of Lcn2-KO mice. The increases in the ratio of eNOS monomers to dimers, and superoxide anion formation were significantly attenuated in mice without lipocalin-2. The level of nitrotyrosine in the total protein and precipitated eNOS of arteries from wide type mice was increased compared with that in Lcn2-KO vessels, despite a similar expression of eNOS protein. The basal and acetylcholine-stimulated superoxide anion production and COX-1 expression were diminished in Lcn2-KO arteries. Replacement with lipocalin-2 in Lcn2-KO mice time-dependently monomerized eNOS in the aorta, increased COX-1 expression levels, and impaired endothelial functions as demonstrated by reduced EDR and enhanced EDC. Lipocalin-2 plays a critical role in the development of obesity-induced endothelial dysfunction through modulation of eNOS activity and oxidative stress.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/PTO-
dc.relation.ispartofBasic & Clinical Pharmacology & Toxicologyen_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectPharmacy and pharmacology environmental studies-
dc.subjectToxicology and environmental safety-
dc.titleLipocalin-2, an inflammatory adipokine, uncouples endothelial nitric-oxide synthase and enhances endothelial dysfunction caused by dietary obesityen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-7835&volume=107, suppl. 1&spage=159&epage=160&date=2010&atitle=Lipocalin-2,+an+inflammatory+adipokine,+uncouples+endothelial+nitric-oxide+synthase+and+enhances+endothelial+dysfunction+caused+by+dietary+obesity-
dc.identifier.emailLiu, JTC: jackyliu@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailLiang, CF: chaofanliang@gmail.comen_HK
dc.identifier.emailLaw, IKM: ivylawkm@graduate.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.hkuros175245en_HK
dc.identifier.volume107, suppl. 1en_HK
dc.identifier.spage159en_HK
dc.identifier.epage160en_HK
dc.description.otherThe 16th World Congress on Basic and Clinical Pharmacology (WorldPharma2010), Copenhagen, Denmark, 17-23 July 2010. In Basic & Clinical Pharmacology & Toxicology, 2010, v. 107, suppl. 1, p. 159-160-

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