Titre
Induction of oxidative stress, lysosome activation and autophagy by nanoparticles in human brain-derived endothelial cells.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Halamoda Kenzaoui, B.
Auteure/Auteur
Chapuis Bernasconi, C.
Auteure/Auteur
Guney-Ayra, S.
Auteure/Auteur
Juillerat-Jeanneret, L.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1470-8728
Statut éditorial
Publié
Date de publication
2012
Volume
441
Numéro
3
Première page
813
Dernière page/numéro d’article
821
Langue
anglais
Résumé
Different types of NPs (nanoparticles) are currently under development for diagnostic and therapeutic applications in the biomedical field, yet our knowledge about their possible effects and fate in living cells is still limited. In the present study, we examined the cellular response of human brain-derived endothelial cells to NPs of different size and structure: uncoated and oleic acid-coated iron oxide NPs (8-9 nm core), fluorescent 25 and 50 nm silica NPs, TiO2 NPs (21 nm mean core diameter) and PLGA [poly(lactic-co-glycolic acid)]-PEO [poly(ethylene oxide)] polymeric NPs (150 nm). We evaluated their uptake by the cells, and their localization, generation of oxidative stress and DNA-damaging effects in exposed cells. We show that NPs are internalized by human brain-derived endothelial cells; however, the extent of their intracellular uptake is dependent on the characteristics of the NPs. After their uptake by human brain-derived endothelial cells NPs are transported into the lysosomes of these cells, where they enhance the activation of lysosomal proteases. In brain-derived endothelial cells, NPs induce the production of an oxidative stress after exposure to iron oxide and TiO2 NPs, which is correlated with an increase in DNA strand breaks and defensive mechanisms that ultimately induce an autophagy process in the cells.
PID Serval
serval:BIB_A753DF5BA629
PMID
Date de création
2012-03-02T10:42:55.687Z
Date de création dans IRIS
2025-05-20T22:42:04Z