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Conference Paper: Lipocalin-2 mediates linoleic acid-induced endothelial dysfunction

TitleLipocalin-2 mediates linoleic acid-induced endothelial dysfunction
Authors
KeywordsBiology
Issue Date2012
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 840.9 How to Cite?
AbstractLipocalin-2, a 25kDa glycoprotein secreted by adipocytes, mediates endothelial dysfunction induced by dietary obesity in mice. The mechanisms underlying the deteriorating effect of lipocalin-2 on endothelial function are not fully understood. The present experiments were designed to explore the role of lipocalin- 2 in endothelial dysfunction caused by fatty acids. Wild type (WT) and lipocalin-2 knock-out (LKO) mice fed with standard chow were injected intraperitoneally with lipocalin-2, alone or in combination with palmitic, oleic or linoleic acid. Carotid arteries were collected to measure endothelium-dependent contractions (EDC) to increasing concentrations of acetylcholine (in the presence of L-NAME). In WT mice, EDC were enhanced significantly by linoleic, but not palmitic or oleic acid, and/or lipocalin-2. On the other hand, LKO mice were irresponsive to either linoleic acid or lipocalin-2 given alone. However, combined administration of linoleic acid andlipocalin-2 in LKO mice resulted in EDC of similar magnitude as in WT mice treated with the combination. Thus, lipocalin-2 permits the deteriorating effect of linoleic acid on endothelial function.
DescriptionSession - 840. Endothelium Dysfunction - Poster: no. 840.9
Persistent Identifierhttp://hdl.handle.net/10722/149226
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorSong, Een_US
dc.contributor.authorFan, Pen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWang, Yen_US
dc.date.accessioned2012-06-22T06:31:01Z-
dc.date.available2012-06-22T06:31:01Z-
dc.date.issued2012en_US
dc.identifier.citationThe 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 840.9en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/149226-
dc.descriptionSession - 840. Endothelium Dysfunction - Poster: no. 840.9-
dc.description.abstractLipocalin-2, a 25kDa glycoprotein secreted by adipocytes, mediates endothelial dysfunction induced by dietary obesity in mice. The mechanisms underlying the deteriorating effect of lipocalin-2 on endothelial function are not fully understood. The present experiments were designed to explore the role of lipocalin- 2 in endothelial dysfunction caused by fatty acids. Wild type (WT) and lipocalin-2 knock-out (LKO) mice fed with standard chow were injected intraperitoneally with lipocalin-2, alone or in combination with palmitic, oleic or linoleic acid. Carotid arteries were collected to measure endothelium-dependent contractions (EDC) to increasing concentrations of acetylcholine (in the presence of L-NAME). In WT mice, EDC were enhanced significantly by linoleic, but not palmitic or oleic acid, and/or lipocalin-2. On the other hand, LKO mice were irresponsive to either linoleic acid or lipocalin-2 given alone. However, combined administration of linoleic acid andlipocalin-2 in LKO mice resulted in EDC of similar magnitude as in WT mice treated with the combination. Thus, lipocalin-2 permits the deteriorating effect of linoleic acid on endothelial function.-
dc.languageengen_US
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_US
dc.subjectBiology-
dc.titleLipocalin-2 mediates linoleic acid-induced endothelial dysfunctionen_US
dc.typeConference_Paperen_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.emailWang, Y: yuwanghk@hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros200112en_US
dc.identifier.volume26-
dc.identifier.issuemeeting abstract-
dc.publisher.placeUnited States-

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