Toxicity of carboxylated carbon nanotubes in endothelial cells is attenuated by stimulation of the autophagic flux with the release of nanomaterial in autophagic vesicles
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.
PubMed
24566271
DOI
10.1016/j.nano.2014.02.001
PII: S1549-9634(14)00035-5
Knihovny.cz E-zdroje
- Klíčová slova
- Autophagy, Bafilomycin A1, Carbon nanotubes, Exocytosis, Microvesicles,
- MeSH
- autofagie fyziologie MeSH
- endoteliální buňky pupečníkové žíly (lidské) MeSH
- endoteliální buňky účinky léků metabolismus MeSH
- exocytóza účinky léků MeSH
- lidé MeSH
- makrolidy farmakologie MeSH
- nanostruktury toxicita MeSH
- nanotrubičky uhlíkové * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
- Názvy látek
- bafilomycin A1 MeSH Prohlížeč
- makrolidy MeSH
- nanotrubičky uhlíkové * MeSH
UNLABELLED: Carbon nanotubes (CNTs) exhibit a number of unique properties that make them attractive for various nanomedicine applications including their intravascular use. Therefore, the vascular toxicity of CNTs is a critical safety concern and methods of CNTs toxicity modulation are of great interest. Here, we report that carboxylated multiwalled carbon nanotubes (MWCNTs) induce a decrease in viability of cultured human umbilical vein endothelial cells (HUVECs) associated with the profound accumulation of autophagosomes. This autophagosome accumulation was mTOR kinase independent and was caused by blockade of the autophagic flux rather than by activation of autophagy. Stimulation of the autophagic flux with 1nmol/L bafilomycin A1 attenuated the cytotoxicity of carboxylated MWCNTs in HUVECs and was associated with the extracellular release of the nanomaterial in autophagic microvesicles. Thus, pharmacological stimulation of the autophagic flux may represent a new method of cytoprotection against toxic effects of nanomaterials. FROM THE CLINICAL EDITOR: This study investigates the mechanisms of toxicity of multiwalled carbon nanutubes on human endothelial cells, concluding that pharmacological stimulation of autophagic flux may represent a new method of cytoprotection against the toxic effects of these nanomaterials.
Center for Biologics Evaluation and Research Food and Drug Administration Rockville MD USA
National Institute of Standards and Technology Gaithersburg MD USA
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