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

Autor: J. Deweirdt, Christelle Guibert, Sabrina Lacomme, I. Baudrimont, Jean-François Quignard, Roger Marthan, Jean-Pierre Savineau, Stéphane Mornet, E. Gontier
Přispěvatelé: Centre de recherche Cardio-Thoracique de Bordeaux [Bordeaux] (CRCTB), Université Bordeaux Segalen - Bordeaux 2-CHU Bordeaux [Bordeaux]-Institut National de la Santé et de la Recherche Médicale (INSERM), Bordeaux Imaging Center (BIC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut François Magendie-Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Institut de Chimie de la Matière Condensée de Bordeaux (ICMCB), Université de Bordeaux (UB)-Institut Polytechnique de Bordeaux-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Service d’Exploration Fonctionnelle Respiratoire, CHU Bordeaux [Bordeaux], Toulin, Stéphane, Université de Bordeaux (UB)-Institut François Magendie-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Archives of Toxicology
Archives of Toxicology, Springer Verlag, 2020, 94 (7), pp.2331-2348. ⟨10.1007/s00204-020-02764-9⟩
Archives of Toxicology, 2020, 94 (7), pp.2331-2348. ⟨10.1007/s00204-020-02764-9⟩
ISSN: 0340-5761
1432-0738
DOI: 10.1007/s00204-020-02764-9⟩
Popis: International audience; 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.
Databáze: OpenAIRE
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