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Conference Paper: Toll-like receptor 4 mediates the vasoconstrictor response initiated by adipose tissue in mice arteries

TitleToll-like receptor 4 mediates the vasoconstrictor response initiated by adipose tissue in mice arteries
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. 413 How to Cite?
AbstractAdipose tissue modulates vascular tone by secreting a number of pro-and anti-inflammatory cytokines including tumour necrosis factor-α (TNFα) and adiponectin, respectively. Toll-like receptor 4 (TLR4) is a major target for lipopolysaccharide and saturated fatty acids, both of which are potent inducers of inflammation. The present study investigated whether or not TLR4 mediates vascular dysfunction induced by obese adipose tissue. Aorta and carotid arteries from 12-week-old wild type mice on standard diet were isolated. White peri-aortic and epididymal adipose tissues from TLR4 mutant mice or wild type littermates fed a high fat diet (HFD) were dissected for ex vivo culture. Isometric tension was measured in artery rings in the absence or presence of conditioned medium collected from the fat explant culture. Several pro- and anti-inflammatory cytokines in adipose tissues were assayed by RT-quantitative PCR. In the presence of N(G)-nitro-L-arginine methyl ester (nitric-oxide synthase inhibitor), epididymal fat from wild type but not TLR4 mutant mice potentiated acetylcholine-mediated endotheliumdependent contraction in carotid arteries. Indomethacin (cyclooxygenase inhibitor) and S18886 (TP receptor antagonist) inhibited the contraction. In addition, inactivation of TLR4 restored the impaired anti-contractrile effect of perivascular fat in aorta caused by HFD feeding. These changes were associated with increased adiponectin expression, but decreased expression of TNFαand interleukin-6 in the adipose tissues of TLR4 mutant mice. Epididymal fat from obese mice facilitates endotheliumdependent contractions to acetylcholine through activation of TLR4, which in turn triggers the release of pro-inflammation cytokines. Perivascular fat from TLR4 mutant mice curtails the contraction possibly by increasing adiponectin.
DescriptionFocused Conference Group: P09 – Nflammation and Immunopharmacology: New Tools for Old Diseases. Paper No. 2335
Persistent Identifierhttp://hdl.handle.net/10722/126867
ISSN
2015 Impact Factor: 3.097
2015 SCImago Journal Rankings: 0.539

 

DC FieldValueLanguage
dc.contributor.authorLiang, CFen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-10-31T12:53:14Z-
dc.date.available2010-10-31T12:53:14Z-
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. 413en_HK
dc.identifier.issn1742-7835-
dc.identifier.urihttp://hdl.handle.net/10722/126867-
dc.descriptionFocused Conference Group: P09 – Nflammation and Immunopharmacology: New Tools for Old Diseases. Paper No. 2335-
dc.description.abstractAdipose tissue modulates vascular tone by secreting a number of pro-and anti-inflammatory cytokines including tumour necrosis factor-α (TNFα) and adiponectin, respectively. Toll-like receptor 4 (TLR4) is a major target for lipopolysaccharide and saturated fatty acids, both of which are potent inducers of inflammation. The present study investigated whether or not TLR4 mediates vascular dysfunction induced by obese adipose tissue. Aorta and carotid arteries from 12-week-old wild type mice on standard diet were isolated. White peri-aortic and epididymal adipose tissues from TLR4 mutant mice or wild type littermates fed a high fat diet (HFD) were dissected for ex vivo culture. Isometric tension was measured in artery rings in the absence or presence of conditioned medium collected from the fat explant culture. Several pro- and anti-inflammatory cytokines in adipose tissues were assayed by RT-quantitative PCR. In the presence of N(G)-nitro-L-arginine methyl ester (nitric-oxide synthase inhibitor), epididymal fat from wild type but not TLR4 mutant mice potentiated acetylcholine-mediated endotheliumdependent contraction in carotid arteries. Indomethacin (cyclooxygenase inhibitor) and S18886 (TP receptor antagonist) inhibited the contraction. In addition, inactivation of TLR4 restored the impaired anti-contractrile effect of perivascular fat in aorta caused by HFD feeding. These changes were associated with increased adiponectin expression, but decreased expression of TNFαand interleukin-6 in the adipose tissues of TLR4 mutant mice. Epididymal fat from obese mice facilitates endotheliumdependent contractions to acetylcholine through activation of TLR4, which in turn triggers the release of pro-inflammation cytokines. Perivascular fat from TLR4 mutant mice curtails the contraction possibly by increasing adiponectin.-
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.titleToll-like receptor 4 mediates the vasoconstrictor response initiated by adipose tissue in mice arteriesen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-7835&volume=107, suppl.1&spage=413&epage=&date=2010&atitle=Toll-like+receptor+4+mediates+the+vasoconstrictor+response+initiated+by+adipose+tissue+in+mice+arteries-
dc.identifier.emailLiang, CF: chaofanliang@gmail.comen_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.hkuros175247en_HK
dc.identifier.volume107, suppl. 1en_HK
dc.identifier.spage413en_HK
dc.identifier.epage413-
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. 413-

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