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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

TitlePharmacological inhibition of adipocyte-fatty acid binding protein (A-FABP) improves endothelial function in male apolipoprotein E-knockout mice
Authors
KeywordsCardiovascular disease
Issue Date2009
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 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
Persistent Identifierhttp://hdl.handle.net/10722/106736
ISSN
2014 SCImago Journal Rankings: 0.104

 

DC FieldValueLanguage
dc.contributor.authorLee, MYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorXu, AMen_HK
dc.date.accessioned2010-09-25T23:28:18Z-
dc.date.available2010-09-25T23:28:18Z-
dc.date.issued2009en_HK
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 P6en_HK
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/106736-
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.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.languageengen_HK
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_HK
dc.subjectCardiovascular disease-
dc.titlePharmacological inhibition of adipocyte-fatty acid binding protein (A-FABP) improves endothelial function in male apolipoprotein E-knockout miceen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLee, MYK: leemary@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailXu, AM: amxu@hkucc.hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros169817en_HK
dc.identifier.volume17en_HK
dc.identifier.issue2en_HK
dc.identifier.spage56en_HK
dc.identifier.epage56-
dc.publisher.placeHong Kong-

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