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J Hazard Mater. 2016 Mar 5;304:186-95. doi: 10.1016/j.jhazmat.2015.10.041. Epub 2015 Oct 26.

Magnetic ferroferric oxide nanoparticles induce vascular endothelial cell dysfunction and inflammation by disturbing autophagy.

Author information

1
College of Bioengineering, Henan University of Technology, Lianhua Street, Zhengzhou 450001, China. Electronic address: chaperones@163.com.
2
College of Bioengineering, Henan University of Technology, Lianhua Street, Zhengzhou 450001, China.
3
Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Abstract

Despite the considerable use of magnetic ferroferric oxide nanoparticles (Fe3O4NPs) worldwide, their safety is still an important topic of debate. In the present study, we detected the toxicity and biological behavior of bare-Fe3O4NPs (B-Fe3O4NPs) on human umbilical vascular endothelial cells (HUVECs). Our results showed that B-Fe3O4NPs did not induce cell death within 24h even at concentrations up to 400 μg/ml. The level of nitric oxide (NO) and the activity of endothelial NO synthase (eNOS) were decreased after exposure to B-Fe3O4NPs, whereas the levels of proinflammatory cytokines were elevated. Importantly, B-Fe3O4NPs increased the accumulation of autophagosomes and LC3-II in HUVECs through both autophagy induction and the blockade of autophagy flux. The levels of Beclin 1 and VPS34, but not phosphorylated mTOR, were increased in the B-Fe3O4NP-treated HUVECs. Suppression of autophagy induction or stimulation of autophagy flux, at least partially, attenuated the B-Fe3O4NP-induced HUVEC dysfunction. Additionally, enhanced autophagic activity might be linked to the B-Fe3O4NP-induced production of proinflammatory cytokines. Taken together, these results demonstrated that B-Fe3O4NPs disturb the process of autophagy in HUVECs, and eventually lead to endothelial dysfunction and inflammation.

KEYWORDS:

Autophagy dysfunction; Endothelial dysfunction; Inflammation; Magnetic ferroferric oxide nanoparticles

PMID:
26551222
DOI:
10.1016/j.jhazmat.2015.10.041
[Indexed for MEDLINE]

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