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

Autor: Lu Zhang, Liuqing Cui, PengFei Qiang, ZhiQiang Chen, YuQi Guo, Hongjuan Jing, YiMing Miao, Xueqin Wang
Rok vydání: 2016
Předmět:
0301 basic medicine
Programmed cell death
Environmental Engineering
Nitric Oxide Synthase Type III
Cell Survival
Health
Toxicology and Mutagenesis
Interleukin-1beta
Apoptosis
Inflammation
02 engineering and technology
Biology
Nitric Oxide
Proinflammatory cytokine
Nitric oxide
03 medical and health sciences
chemistry.chemical_compound
Microscopy
Electron
Transmission
Autophagy
Human Umbilical Vein Endothelial Cells
medicine
Humans
Environmental Chemistry
Endothelial dysfunction
Magnetite Nanoparticles
Waste Management and Disposal
Cells
Cultured
L-Lactate Dehydrogenase
Tumor Necrosis Factor-alpha
021001 nanoscience & nanotechnology
medicine.disease
Pollution
Cell biology
Endothelial stem cell
C-Reactive Protein
030104 developmental biology
chemistry
Immunology
Endothelium
Vascular
medicine.symptom
0210 nano-technology
Zdroj: Journal of Hazardous Materials. 304:186-195
ISSN: 0304-3894
DOI: 10.1016/j.jhazmat.2015.10.041
Popis: 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.
Databáze: OpenAIRE
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