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Article: A-FABP and oxidative stress underlie the impairment of endothelium-dependent relaxations to serotonin and the intima-medial thickening in the porcine coronary artery with regenerated endothelium

TitleA-FABP and oxidative stress underlie the impairment of endothelium-dependent relaxations to serotonin and the intima-medial thickening in the porcine coronary artery with regenerated endothelium
Authors
KeywordsApocynin
BMS309403
Bradykinin
Endothelial cells
Gi proteins
Issue Date2013
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/page/acncdm/about.html
Citation
ACS Chemical Neuroscience, 2013, v. 4 n. 1, p. 122-129 How to Cite?
AbstractExperiments were designed to determine the cause of the selective dysfunction of G(i) proteins, characterized by a reduced endothelium-dependent relaxation to serotonin (5-hydroxytryptamine), in coronary arteries lined with regenerated endothelial cells. Part of the endothelium of the left anterior descending coronary artery of female pigs was removed in vivo to induce regeneration. The animals were treated chronically with vehicle (control), apocynin (antioxidant), or BMS309403 (A-FABP inhibitor) for 28 days before functional examination and histological analysis of segments of coronary arteries with native or regenerated endothelium of the same hearts. Isometric tension was recorded in organ chambers and cumulative concentration-relaxation curves obtained in response to endothelium-dependent [serotonin (G(i) protein mediated activation of eNOS) and bradykinin (G(q) protein mediated activation of eNOS)] and independent [detaNONOate (cGMP-mediated), isoproterenol (cAMP-mediated)] vasodilators. The two inhibitors tested did not acutely affect relaxations of preparations with either native or regenerated endothelium. In the chronically treated groups, however, both apocynin and BMS309403 abolished the reduction in relaxation to serotonin in segments covered with regenerated endothelium and prevented the intima-medial thickening caused by endothelial regeneration, without affecting responses to bradykinin or endothelium-independent agonists (detaNONOate and isoproterenol). Thus, inhibition of either oxidative stress or A-FABP likely prevents both the selective dysfunction of G(i) protein mediated relaxation to serotonin and the neointimal thickening resulting from endothelial regeneration. © 2012 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/181056
ISSN
2015 Impact Factor: 4.348
2015 SCImago Journal Rankings: 1.842
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, CKen_US
dc.contributor.authorZhao, Yen_US
dc.contributor.authorLiao, SYen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLee, MYKen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2013-02-19T11:32:47Z-
dc.date.available2013-02-19T11:32:47Z-
dc.date.issued2013en_US
dc.identifier.citationACS Chemical Neuroscience, 2013, v. 4 n. 1, p. 122-129en_US
dc.identifier.issn1948-7193-
dc.identifier.urihttp://hdl.handle.net/10722/181056-
dc.description.abstractExperiments were designed to determine the cause of the selective dysfunction of G(i) proteins, characterized by a reduced endothelium-dependent relaxation to serotonin (5-hydroxytryptamine), in coronary arteries lined with regenerated endothelial cells. Part of the endothelium of the left anterior descending coronary artery of female pigs was removed in vivo to induce regeneration. The animals were treated chronically with vehicle (control), apocynin (antioxidant), or BMS309403 (A-FABP inhibitor) for 28 days before functional examination and histological analysis of segments of coronary arteries with native or regenerated endothelium of the same hearts. Isometric tension was recorded in organ chambers and cumulative concentration-relaxation curves obtained in response to endothelium-dependent [serotonin (G(i) protein mediated activation of eNOS) and bradykinin (G(q) protein mediated activation of eNOS)] and independent [detaNONOate (cGMP-mediated), isoproterenol (cAMP-mediated)] vasodilators. The two inhibitors tested did not acutely affect relaxations of preparations with either native or regenerated endothelium. In the chronically treated groups, however, both apocynin and BMS309403 abolished the reduction in relaxation to serotonin in segments covered with regenerated endothelium and prevented the intima-medial thickening caused by endothelial regeneration, without affecting responses to bradykinin or endothelium-independent agonists (detaNONOate and isoproterenol). Thus, inhibition of either oxidative stress or A-FABP likely prevents both the selective dysfunction of G(i) protein mediated relaxation to serotonin and the neointimal thickening resulting from endothelial regeneration. © 2012 American Chemical Society.-
dc.languageengen_US
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/page/acncdm/about.html-
dc.relation.ispartofACS Chemical Neuroscienceen_US
dc.subjectApocynin-
dc.subjectBMS309403-
dc.subjectBradykinin-
dc.subjectEndothelial cells-
dc.subjectGi proteins-
dc.titleA-FABP and oxidative stress underlie the impairment of endothelium-dependent relaxations to serotonin and the intima-medial thickening in the porcine coronary artery with regenerated endotheliumen_US
dc.typeArticleen_US
dc.identifier.emailChan, CK: calvinc2@hku.hken_US
dc.identifier.emailZhao, Y: aprilzyz@hku.hken_US
dc.identifier.emailLiao, SY: lsy923@hkucc.hku.hken_US
dc.identifier.emailLee, MYK: leemary@hkucc.hku.hken_US
dc.identifier.emailXu, A: amxu@hku.hk-
dc.identifier.emailTse, HF: hftse@hku.hk-
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hk-
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1021/cn3000873-
dc.identifier.pmid23336051-
dc.identifier.pmcidPMC3547481-
dc.identifier.scopuseid_2-s2.0-84872525236-
dc.identifier.hkuros213280en_US
dc.identifier.hkuros215867-
dc.identifier.volume4en_US
dc.identifier.issue1-
dc.identifier.spage122en_US
dc.identifier.epage129en_US
dc.identifier.isiWOS:000313920600018-
dc.publisher.placeUnited States-

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