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dc.rights.licenseopenen_US
hal.structure.identifierEnvironnements et Paléoenvironnements OCéaniques [EPOC]
dc.contributor.authorGERMANDE, Ophelie
dc.contributor.authorDUCRET, Thomas
dc.contributor.authorQUIGNARD, Jean-Francois
dc.contributor.authorDEWEIRDT, Juliette
dc.contributor.authorFREUND-MICHEL, Véronique
dc.contributor.authorERRERA, Marie-Hélène
dc.contributor.authorCARDOUAT, Guillaume
dc.contributor.authorVACHER, Pierre
dc.contributor.authorMULLER, Bernard
dc.contributor.authorBERGER, Patrick
dc.contributor.authorGUIBERT, Christelle
dc.contributor.authorBAUDRIMONT, Magalie
IDREF: 105696722
hal.structure.identifierEnvironnements et Paléoenvironnements OCéaniques [EPOC]
dc.contributor.authorBAUDRIMONT, Magalie
IDREF: 105696722
dc.contributor.authorBAUDRIMONT, Isabelle
dc.date.accessioned2023-06-16T12:18:53Z
dc.date.available2023-06-16T12:18:53Z
dc.date.issued2022-04-26
dc.identifier.issn2076-3921en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/182707
dc.description.abstractEnThe development and use of nanomaterials, especially of nickel oxide nanoparticles (NiONPs), is expected to provide many benefits but also has raised concerns about the potential human health risks. Inhaled NPs are known to exert deleterious cardiovascular side effects, including pulmonary hypertension. Consequently, patients with pulmonary hypertension (PH) could be at increased risk for morbidity. The objective of this study was to compare the toxic effects of NiONPs on human pulmonary artery endothelial cells (HPAEC) under physiological and pathological conditions. The study was conducted with an in vitro model mimicking the endothelial dysfunction observed in PH. HPAEC were cultured under physiological (static and normoxic) or pathological (20% cycle stretch and hypoxia) conditions and exposed to NiONPs (0.5–5 μg/cm2) for 4 or 24 h. The following endpoints were studied: (i) ROS production using CM-H2DCF-DA and MitoSOX probes, (ii) nitrite production by the Griess reaction, (iii) IL-6 secretion by ELISA, (iv) calcium signaling with a Fluo-4 AM probe, and (v) mitochondrial dysfunction with TMRM and MitoTracker probes. Our results evidenced that under pathological conditions, ROS and nitrite production, IL-6 secretions, calcium signaling, and mitochondria alterations increased compared to physiological conditions. Human exposure to NiONPs may be associated with adverse effects in vulnerable populations with cardiovascular risks.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enendothelial dysfunction; calcium
dc.subject.encyclic stretch
dc.subject.enhuman pulmonary artery endothelial cells
dc.subject.ennickel oxide nanoparticles
dc.subject.enmitochondria alteration
dc.subject.enreactive oxygen species
dc.title.enNiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/antiox11050847en_US
dc.subject.halSciences de l'environnementen_US
bordeaux.journalAntioxidantsen_US
bordeaux.volume11en_US
bordeaux.hal.laboratoriesEPOC : Environnements et Paléoenvironnements Océaniques et Continentaux - UMR 5805en_US
bordeaux.issue5en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.teamEAen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Antioxidants&rft.date=2022-04-26&rft.volume=11&rft.issue=5&rft.eissn=2076-3921&rft.issn=2076-3921&rft.au=GERMANDE,%20Ophelie&DUCRET,%20Thomas&QUIGNARD,%20Jean-Francois&DEWEIRDT,%20Juliette&FREUND-MICHEL,%20V%C3%A9ronique&rft.genre=article


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