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Conference Paper: Pharmacological inhibition of adipocyte-fatty acid binding protein (A-FABP) improves endothelial function in male apolipoprotein E-knockout mice
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TitlePharmacological inhibition of adipocyte-fatty acid binding protein (A-FABP) improves endothelial function in male apolipoprotein E-knockout mice
 
AuthorsLee, MYK
Vanhoutte, PM
Xu, AM
 
KeywordsCardiovascular disease
 
Issue Date2009
 
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
 
CitationThe 13th Annual Scientific Meeting Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 56, abstract P6 [How to Cite?]
 
AbstractAdipocyte-fatty acid binding protein (A-FABP) modulates inflammatory responses in macrophages and may play a role in formation of foam cells and atherosclerotic plaques. A-FABP is markedly upregulated in regenerated porcine coronary arterial endothelial cells. The project were designed to investigate the presence (or not) of A-FABP as well as endothelial function at early stages of atherosclerosis in the aorta of 8, 12 and 18 weeks old male C57 apolipoprotein E-knockout (ApoE-/-) mice. The effect was determined by treatment with a selective A-FABP inhibitor, BMS 309403, in 12-weeks old ApoE-/- mice. A-FABP was detected by immunoflorescent staining in the endothelium of the aorta at 12, but not 8 weeks. In myograph experiments, the endothelium-dependent relaxations to acetylcholine and UK14304 (a selective α2-adrenoceptor agonist) were reduced significantly in the ApoE-/- mice at 8 and 12 weeks on, respectively, compared to those obtained in wild type mice. Relaxations to the calcium ionophore A23187 were diminished significantly only from 18 weeks. Treatment with the A-FABP inhibitor significantly improved the relaxation to acetylcholine and UK14304 but not that to A23187 without affecting the plasma lipid profile. In conclusion, A-FABP was detected in male atherosclerotic-prone ApoE-/- mice since the age of 12 weeks. Endothelial dysfunction was observed as early as at 8 weeks of age and deteriorated until 18 weeks, as judged from the reduced relaxations to acetylcholine, UK14304 and A23187. Endothelial dysfunction can be alleviated by treatment with an A-FABP inhibitor, suggesting that A-FABP may be a novel target for the treatment of endothelial dysfunction.
 
DescriptionThis journal issue contain abstracts of the 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine 2009
Abstracts for Posters: P6
 
ISSN1027-7811
2013 SCImago Journal Rankings: 0.104
 
DC FieldValue
dc.contributor.authorLee, MYK
 
dc.contributor.authorVanhoutte, PM
 
dc.contributor.authorXu, AM
 
dc.date.accessioned2010-09-25T23:28:18Z
 
dc.date.available2010-09-25T23:28:18Z
 
dc.date.issued2009
 
dc.description.abstractAdipocyte-fatty acid binding protein (A-FABP) modulates inflammatory responses in macrophages and may play a role in formation of foam cells and atherosclerotic plaques. A-FABP is markedly upregulated in regenerated porcine coronary arterial endothelial cells. The project were designed to investigate the presence (or not) of A-FABP as well as endothelial function at early stages of atherosclerosis in the aorta of 8, 12 and 18 weeks old male C57 apolipoprotein E-knockout (ApoE-/-) mice. The effect was determined by treatment with a selective A-FABP inhibitor, BMS 309403, in 12-weeks old ApoE-/- mice. A-FABP was detected by immunoflorescent staining in the endothelium of the aorta at 12, but not 8 weeks. In myograph experiments, the endothelium-dependent relaxations to acetylcholine and UK14304 (a selective α2-adrenoceptor agonist) were reduced significantly in the ApoE-/- mice at 8 and 12 weeks on, respectively, compared to those obtained in wild type mice. Relaxations to the calcium ionophore A23187 were diminished significantly only from 18 weeks. Treatment with the A-FABP inhibitor significantly improved the relaxation to acetylcholine and UK14304 but not that to A23187 without affecting the plasma lipid profile. In conclusion, A-FABP was detected in male atherosclerotic-prone ApoE-/- mice since the age of 12 weeks. Endothelial dysfunction was observed as early as at 8 weeks of age and deteriorated until 18 weeks, as judged from the reduced relaxations to acetylcholine, UK14304 and A23187. Endothelial dysfunction can be alleviated by treatment with an A-FABP inhibitor, suggesting that A-FABP may be a novel target for the treatment of endothelial dysfunction.
 
dc.description.naturelink_to_OA_fulltext
 
dc.descriptionThis journal issue contain abstracts of the 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine 2009
 
dc.descriptionAbstracts for Posters: P6
 
dc.identifier.citationThe 13th Annual Scientific Meeting Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 56, abstract P6 [How to Cite?]
 
dc.identifier.epage56
 
dc.identifier.hkuros169817
 
dc.identifier.issn1027-7811
2013 SCImago Journal Rankings: 0.104
 
dc.identifier.issue2
 
dc.identifier.spage56
 
dc.identifier.urihttp://hdl.handle.net/10722/106736
 
dc.identifier.volume17
 
dc.languageeng
 
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
 
dc.publisher.placeHong Kong
 
dc.relation.ispartofJournal of the Hong Kong College of Cardiology
 
dc.subjectCardiovascular disease
 
dc.titlePharmacological inhibition of adipocyte-fatty acid binding protein (A-FABP) improves endothelial function in male apolipoprotein E-knockout mice
 
dc.typeConference_Paper
 
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