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Conference Paper: Endothelium-dependent contractions induced by aging and diet-induced obesity are attenuated in lipocalin-2 deficient mice

TitleEndothelium-dependent contractions induced by aging and diet-induced obesity are attenuated in lipocalin-2 deficient mice
Authors
Issue Date2010
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The Experimental Biology 2010, Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 570.3 How to Cite?
AbstractAIM: Levels of Lipocalin-2, a pro-inflammatory adipokine, correlates with adiposity, dyslipidemia, hyperglycemia and insulin resistance. The present study evaluates vascular function in mice with deletion of the lipocalin-2 gene (Lcn2-KO). METHODS: Wild type (WT) and Lcn2-KO mice were fed with standard or high fat diet for 3–17 weeks. Intra-arterial blood pressure was measured. Isometric tension was measured in carotid artery rings with or without endothelium. Protein expression was measured by Western blotting. RESULTS: The obesity-induced increase in systolic blood pressure was attenuated in Lcn2-KO mice. In aged or obese WT mice, acetylcholine (ACh)-elicited endothelium-dependent contractions were abolished by the COX-1 selective inhibitor SC560 and the NADH oxidase inhibitor diphenylene iodonium. These contractions were attenuated in Lcn2-KO mice. ACh-stimulated superoxide anion production, COX-1 mRNA and protein expression were decreased in Lcn2-KO arteries. ACh-induced production of prostacyclins (PGI2) was lower in Lcn2-KO preparations. In aged or obese WT mice, PGI2 caused contractions in rings without endothelium but these contractions were reversed to relaxations in Lcn2-KO arteries. CONCLUSIONS: Lipocalin-2 plays an important role in obesity-induced hypertension and endothelial dysfunction through production of superoxide anions and COX-1 expression.
Persistent Identifierhttp://hdl.handle.net/10722/106847
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorLiu, JTCen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorMak, TWen_HK
dc.contributor.authorLaw, IKMen_HK
dc.contributor.authorLiang, CFen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorWang, Yen_HK
dc.date.accessioned2010-09-25T23:32:53Z-
dc.date.available2010-09-25T23:32:53Z-
dc.date.issued2010en_HK
dc.identifier.citationThe Experimental Biology 2010, Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 570.3en_HK
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/106847-
dc.description.abstractAIM: Levels of Lipocalin-2, a pro-inflammatory adipokine, correlates with adiposity, dyslipidemia, hyperglycemia and insulin resistance. The present study evaluates vascular function in mice with deletion of the lipocalin-2 gene (Lcn2-KO). METHODS: Wild type (WT) and Lcn2-KO mice were fed with standard or high fat diet for 3–17 weeks. Intra-arterial blood pressure was measured. Isometric tension was measured in carotid artery rings with or without endothelium. Protein expression was measured by Western blotting. RESULTS: The obesity-induced increase in systolic blood pressure was attenuated in Lcn2-KO mice. In aged or obese WT mice, acetylcholine (ACh)-elicited endothelium-dependent contractions were abolished by the COX-1 selective inhibitor SC560 and the NADH oxidase inhibitor diphenylene iodonium. These contractions were attenuated in Lcn2-KO mice. ACh-stimulated superoxide anion production, COX-1 mRNA and protein expression were decreased in Lcn2-KO arteries. ACh-induced production of prostacyclins (PGI2) was lower in Lcn2-KO preparations. In aged or obese WT mice, PGI2 caused contractions in rings without endothelium but these contractions were reversed to relaxations in Lcn2-KO arteries. CONCLUSIONS: Lipocalin-2 plays an important role in obesity-induced hypertension and endothelial dysfunction through production of superoxide anions and COX-1 expression.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleEndothelium-dependent contractions induced by aging and diet-induced obesity are attenuated in lipocalin-2 deficient miceen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=24, Meeting abstracts suppl., abstract no. 570.3&spage=&epage=&date=2010&atitle=Endothelium-dependent+contractions+induced+by+aging+and+diet-induced+obesity+are+attenuated+in+lipocalin-2+deficient+mice-
dc.identifier.emailLiu, JTC: jackyliu@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailLaw, IKM: ivylawkm@graduate.hku.hken_HK
dc.identifier.emailLiang, CF: chaofanliang@gmail.comen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.hkuros170023en_HK
dc.identifier.volume24en_HK
dc.identifier.issueMeeting abstract suppl.-
dc.description.otherThe Experimental Biology 2010, Anaheim, CA., 24-28 April 2010. In The FASEB Journal, 2010, v. 24 Meeting abstract suppl., abstract no. 570.3-

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