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dc.rights.licenseopenen_US
dc.contributor.authorBARRIER, Marjorie
dc.contributor.authorBÉGORRE, Marc-Antoine
dc.contributor.authorBAUDRIMONT, Isabelle
dc.contributor.authorDUBOIS, Mathilde
dc.contributor.authorFREUND-MICHEL, Véronique
dc.contributor.authorMARTHAN, Roger
dc.contributor.authorSAVINEAU, Jean-Pierre
dc.contributor.authorMULLER, Bernard
hal.structure.identifierUnité de Recherche Oenologie [Villenave d'Ornon] [OENO]
dc.contributor.authorCOURTOIS, Arnaud
IDREF: 092021301
dc.date.accessioned2021-05-31T14:53:58Z
dc.date.available2021-05-31T14:53:58Z
dc.date.issued2016-04-01
dc.identifier.issn1879-3177en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/78773
dc.descriptionArticle cliniqueen_US
dc.description.abstractEnParticulate air pollution exerts deleterious effects on cardiovascular system. We previously described that exposure to urban particulate matter (SRM1648) impairs nitric oxide (NO, a major vasculoprotective factor) responsiveness in intrapulmonary arteries. As Heme Oxygenase-1 (HO-1) is induced by urban particles in some cell types and is known to alter NO-dependent signaling pathway, the objective was to characterize HO-1 involvement in SRM1648-induced impairment of NO-dependent relaxation in intrapulmonary arteries. Rat intrapulmonary artery rings were exposed or not to Co (III) Protoporphyrin IX Chloride (HO-1 inducer) or SRM1648 in the absence or presence of Cr (III) Mesoporphyrin IX Chloride (HO-1 activity inhibitor). NO-dependent relaxation was assessed with DEA-NOnoate (DEA-NO) on pre-contracted arteries. HO-1 and soluble guanylyl-cyclase (sGC) mRNA and protein expressions were assessed by qRT-PCR and Western blotting, respectively. SRM1648 or Co (III) Protoporphyrin IX Chloride exposure (24) impaired DEA-NO-dependent relaxation. The SRM-induced alteration of DEA-NO responsiveness was partially prevented by Cr (III) Mesoporphyrin IX Chloride. Co (III) Protoporphyrin IX Chloride induced HO-1 mRNA and protein expressions, whereas SRM1648 only induced HO-1 protein expression without affecting its mRNA level. Exposure to either SRM1648 or to Co (III) Protoporphyrin IX Chloride did not affect the expression levels of sGC. In conclusion, this study provides some evidence that impairment of NO signaling pathway in intrapulmonary arteries involves HO-1. Therefore it highlights the role of HO-1 in particulate matter-induced detrimental effects in pulmonary circulation.
dc.language.isoENen_US
dc.subject.enAir Pollutants
dc.subject.enAnimals
dc.subject.enHeme Oxygenase (Decyclizing)
dc.subject.enIn Vitro Techniques
dc.subject.enMale
dc.subject.enNitric Oxide
dc.subject.enParticulate Matter
dc.subject.enProtoporphyrins
dc.subject.enPulmonary Artery
dc.subject.enRats
dc.subject.enWistar
dc.subject.enVasodilation
dc.title.enInvolvement of Heme Oxygenase-1 in particulate matter-induced impairment of NO-dependent relaxation in rat intralobar pulmonary arteries.
dc.title.alternativeToxicol In Vitroen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.tiv.2016.01.005en_US
dc.subject.halSciences du Vivant [q-bio]/Biologie végétaleen_US
dc.identifier.pubmed26780163en_US
bordeaux.journalToxicology in Vitroen_US
bordeaux.page205-11en_US
bordeaux.volume32en_US
bordeaux.hal.laboratoriesUnité de Recherche Oenologie - EA 4577en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionINRAEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-03243608
hal.version1
hal.date.transferred2021-05-31T14:54:04Z
hal.exporttrue
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