GERMANDE, Ophelie; DUCRET, Thomas; QUIGNARD, Jean-Francois; DEWEIRDT, Juliette; FREUND-MICHEL, Véronique; ERRERA, Marie-Hélène; CARDOUAT, Guillaume; VACHER, Pierre; MULLER, Bernard; BERGER, Patrick; GUIBERT, Christelle; BAUDRIMONT, Magalie; BAUDRIMONT, Magalie; BAUDRIMONT, Isabelle

doi:10.3390/antiox11050847

Environnements et Paléoenvironnements OCéaniques [EPOC]

DUCRET, Thomas

QUIGNARD, Jean-Francois

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Article de revue

Ce document a été publié dans

Antioxidants. 2022-04-26, vol. 11, n° 5

Résumé en anglais

The 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.< Réduire

Mots clés en anglais

endothelial dysfunction; calcium

cyclic stretch

human pulmonary artery endothelial cells

nickel oxide nanoparticles

mitochondria alteration

reactive oxygen species

URI

https://oskar-bordeaux.fr/handle/20.500.12278/182707

DOI

http://dx.doi.org/10.3390/antiox11050847

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EPOC : Environnements et Paléoenvironnements Océaniques et Continentaux - UMR 5805

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NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction

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