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Graphene quantum dots induce apoptosis, autophagy, and inflammatory response via p38 mitogen-activated protein kinase and nuclear factor-κB mediated signaling pathways in activated THP-1 macrophages.

Qin,Y, Zhou,ZW, Pan,ST, He,ZX, Zhang,X, Qiu,JX, Duan,W, Yang,T and Zhou,SF 2015, Graphene quantum dots induce apoptosis, autophagy, and inflammatory response via p38 mitogen-activated protein kinase and nuclear factor-κB mediated signaling pathways in activated THP-1 macrophages., Toxicology, vol. 327, pp. 62-76, doi: 10.1016/j.tox.2014.10.011.

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Title Graphene quantum dots induce apoptosis, autophagy, and inflammatory response via p38 mitogen-activated protein kinase and nuclear factor-κB mediated signaling pathways in activated THP-1 macrophages.
Author(s) Qin,Y
Zhou,ZW
Pan,ST
He,ZX
Zhang,X
Qiu,JX
Duan,W
Yang,T
Zhou,SF
Journal name Toxicology
Volume number 327
Start page 62
End page 76
Publisher Elsevier
Place of publication Ireland
Publication date 2015
ISSN 1879-3185
Keyword(s) Autophagy
Graphene quantum dot
Inflammation
Nanotoxicity
Programmed cell death
Science & Technology
Life Sciences & Biomedicine
Pharmacology & Pharmacy
Toxicology
HEXAGONAL BORON-NITRIDE
OXIDATIVE STRESS
UP-CONVERSION
FUNCTIONALIZED GRAPHENE
COMPOSITE-MATERIALS
STEM-CELLS
IN-VITRO
OXIDE
SIZE
Summary The biomedical application of graphene quantum dots (GQDs) is a new emerging area. However, their safety data are still in scarcity to date. Particularly, the effect of GQDs on the immune system remains unknown. This study aimed to elucidate the interaction of GQDs with macrophages and the underlying mechanisms. Our results showed that GQDs slightly affected the cell viability and membrane integrity of macrophages, whereas GQDs significantly increased reactive oxygen species (ROS) generation and apoptotic and autophagic cell death with an increase in the expression level of Bax, Bad, caspase 3, caspase 9, beclin 1, and LC3-I/II and a decrease in that of Bcl-2. Furthermore, low concentrations of GQDs significantly increased the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-8, whereas high concentrations of GQDs elicited opposite effects on the cytokines production. SB202190, a selective inhibitor of p38 mitogen-activated protein kinase (MAPK), abolished the cytokine-inducing effect of GQDs in macrophages. Moreover, GQDs significantly increased the phosphorylation of p38 MAPK and p65, and promoted the nuclear translocation of nuclear factor-κB (NF-κB). Taken together, these results show that GQDs induce ROS generation, apoptosis, autophagy, and inflammatory response via p38MAPK and NF-κB mediated signaling pathways in THP-1 activated macrophages.
Language eng
DOI 10.1016/j.tox.2014.10.011
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 929999 Health not elsewhere classified
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2015, Elsevier
Persistent URL http://hdl.handle.net/10536/DRO/DU:30072035

Document type: Journal Article
Collection: School of Medicine
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