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Toxicity of carboxylated carbon nanotubes in endothelial cells is attenuated by stimulation of the autophagic flux associated with the release of nanomaterial in autophagic vesicles

Published

Author(s)

Martina Orecna, Silvia De Paoli Lacerda, Olga Janouskova, Tseday Tegegn, Marcela Filapova, John E. Bonevich, Jan Simak

Abstract

Here, we present a new method for the pharmacological modulation of the vascular toxicity of carbon nanotubes. We report that carboxylated multiwalled carbon nanotubes (MWCNTs) induce autophagosome accumulation in cultured human umbilical vein endothelial cells (HUVECs) which is caused by blockade of the autophagic flux. Stimulation of the autophagic flux with 1 nM bafilomycin A1 (BafA1) attenuated the cytotoxicity of carboxylated MWCNTs in HUVECs and was associated with the exocytosis of nanotubes in autophagic vesicles.
Citation
Nanomedicine: nanotechnology, biology, and medicine
Volume
10
Issue
5

Keywords

carbon nanotubes, autophagy, bafilomycin A1, microvesicles

Citation

Orecna, M. , De, S. , Janouskova, O. , Tegegn, T. , Filapova, M. , Bonevich, J. and Simak, J. (2014), Toxicity of carboxylated carbon nanotubes in endothelial cells is attenuated by stimulation of the autophagic flux associated with the release of nanomaterial in autophagic vesicles, Nanomedicine: nanotechnology, biology, and medicine, [online], https://doi.org/10.1016/j.nano.2014.02.001 (Accessed July 31, 2021)
Created July 1, 2014, Updated November 10, 2018