DEWEIRDT, Juliette; QUIGNARD, Jean-François; LACOMME, Sabrina; GONTIER, Etienne; MORNET, Stéphane; SAVINEAU, Jean-Pierre; MARTHAN, Roger; GUIBERT, Christelle; BAUDRIMONT, Isabelle

doi:10.1007/s00204-020-02764-9

Métadonnées

Afficher la notice complète

Licence d’utilisation du document

DEWEIRDT, Juliette
Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] [CRCTB]

QUIGNARD, Jean-François
Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] [CRCTB]

LACOMME, Sabrina
Bordeaux Imaging Center [BIC]

Langue

Article de revue

Ce document a été publié dans

Archives of Toxicology. 2020, vol. 94, n° 7, p. 2331-2348

Springer Verlag

Résumé en anglais

Human exposure to manufactured nanoparticles (NPs) is a public health concern. Endothelial cells lining the inner surface of arteries could be one of the primary targets for inhaled nanoparticles. Moreover, it is well known that alteration in calcium signaling is a critical event involved in the physiopathology of cardiovascular diseases. The objective of this study was to assess the role of oxidative stress in carbon black FW2 NPs-induced alteration in calcium signaling and mitochondria in human pulmonary artery endothelial cells. To this end, cells were exposed for 4 or 24 h to FW2 NPs (1–10 μg/cm2) and the following endpoints were studied: (i) production of ROS by fluorimetry and electron paramagnetic resonance, (ii) variation in intracellular calcium concentration by confocal microscopy, and (iii) mitochondrial alteration and apoptosis by confocal microscopy and transmission electronic microscopy. Exposure to FW2 NPs concentration-dependently increases oxidative stress, evidenced by the production of superoxide anion leading to an alteration in calcium content of intracellular organelles, such as endoplasmic reticulum and mitochondria activating, in turn, intrinsic apoptosis. This study provides evidence that FW2 NPs exposure impairs calcium signaling and mitochondria triggered by oxidative stress, and, thus, could act as a cardiovascular disease risk owing to the key role of calcium homeostasis in the control of vascular tone.< Réduire

DOI

http://dx.doi.org/10.1007/s00204-020-02764-9

Origine

Importé de hal

Métadonnées

Licence d’utilisation du document

In vitro study of carbon black nanoparticles on human pulmonary artery endothelial cells: effects on calcium signaling and mitochondrial alterations

Langue

Ce document a été publié dans

Résumé en anglais

DOI

Origine

Unités de recherche