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Article: Dysfunction of the nitric oxide pathway during coronary endothelium regeneration | Dysfonction de la voie du monoxyde d'azote au cours de la régénération de l'endothélium coronarien.

TitleDysfunction of the nitric oxide pathway during coronary endothelium regeneration | Dysfonction de la voie du monoxyde d'azote au cours de la régénération de l'endothélium coronarien.
Authors
Issue Date2002
Citation
Bulletin De LAcademie Nationale De Medecine, 2002, v. 186 n. 8, p. 1525-1539; discussion 1540 How to Cite?
AbstractExperiments were designed to determine whether or not aging per se or cellular density affects endothelial NO-synthase (eNOS) activity in cultured coronary endothelial cells of the pig. A diminished activity could explain the reduced endothelium-dependent relaxation to bradykinin previously observed during regeneration after endothelial injury. The results demonstrate that cell cultures derived from eight-day old regenerated endothelium exhibit a normal basal production of cyclic GMP, but a reduced response to bradykinin or the Ca2+ ionophore A23187. With multiple cellular passages, used to mimick aging, the basal production of cyclic GMP remained stable during the first passage, to decrease moderately after one month (4th passage). By contrast, the response to bradykinin was reduced as of the second passage, to remain stable thereafter. In cultured aortic endothelial cells, an increase in cellular density was accompanied by a reduced number of active eNOS-site, as well as a reduction of NO production in the response to both bradykinin and A23187. These results suggest that both the increased cellular density and cell senescence explain the endothelial dysfunction during regeneration. They permit a better understanding of the changes in vascular reactivity in the course of endothelial regeneration, and of its pathological consequences.
Persistent Identifierhttp://hdl.handle.net/10722/171302
ISSN
2014 Impact Factor: 0.085
2015 SCImago Journal Rankings: 0.114
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorFournetBourguignon, MPen_US
dc.contributor.authorVilaine, JPen_US
dc.date.accessioned2012-10-30T06:13:16Z-
dc.date.available2012-10-30T06:13:16Z-
dc.date.issued2002en_US
dc.identifier.citationBulletin De LAcademie Nationale De Medecine, 2002, v. 186 n. 8, p. 1525-1539; discussion 1540en_US
dc.identifier.issn0001-4079en_US
dc.identifier.urihttp://hdl.handle.net/10722/171302-
dc.description.abstractExperiments were designed to determine whether or not aging per se or cellular density affects endothelial NO-synthase (eNOS) activity in cultured coronary endothelial cells of the pig. A diminished activity could explain the reduced endothelium-dependent relaxation to bradykinin previously observed during regeneration after endothelial injury. The results demonstrate that cell cultures derived from eight-day old regenerated endothelium exhibit a normal basal production of cyclic GMP, but a reduced response to bradykinin or the Ca2+ ionophore A23187. With multiple cellular passages, used to mimick aging, the basal production of cyclic GMP remained stable during the first passage, to decrease moderately after one month (4th passage). By contrast, the response to bradykinin was reduced as of the second passage, to remain stable thereafter. In cultured aortic endothelial cells, an increase in cellular density was accompanied by a reduced number of active eNOS-site, as well as a reduction of NO production in the response to both bradykinin and A23187. These results suggest that both the increased cellular density and cell senescence explain the endothelial dysfunction during regeneration. They permit a better understanding of the changes in vascular reactivity in the course of endothelial regeneration, and of its pathological consequences.en_US
dc.languageengen_US
dc.relation.ispartofBulletin de l"Academie nationale de medecineen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCoronary Vessels - Metabolism - Physiologyen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Metabolism - Physiologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Metabolismen_US
dc.subject.meshRegenerationen_US
dc.subject.meshSwineen_US
dc.titleDysfunction of the nitric oxide pathway during coronary endothelium regeneration | Dysfonction de la voie du monoxyde d'azote au cours de la régénération de l'endothélium coronarien.en_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid12669367-
dc.identifier.scopuseid_2-s2.0-0141798836en_US
dc.identifier.volume186en_US
dc.identifier.issue8en_US
dc.identifier.spage1525en_US
dc.identifier.epage1539; discussion 1540en_US
dc.identifier.isiWOS:000181182800015-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridFournetBourguignon, MP=6507287770en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US

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