Publication: Intracellular nickel accumulation induces apoptosis and cell cycle arrest in human astrocytic cells
2
item.page.dc.date.issued
2021-01-16
item.page.dc.type
item.page.dc.identifier.issn
1756591X
item.page.dc.identifier.doi
item.page.dc.identifier.other
2-s2.0-85101469556
item.page.dc.rights
Mahidol University
item.page.dc.rights.holder
SCOPUS
item.page.dc.identifier.citation
Metallomics : integrated biometal science. Vol.13, No.1 (2021)
punsarn.item.page.citation
Ruedeemars Yubolphan, Suttinee Phuagkhaopong, Kant Sangpairoj, Nathawut Sibmooh, Christopher Power, Pornpun Vivithanaporn Intracellular nickel accumulation induces apoptosis and cell cycle arrest in human astrocytic cells. Metallomics : integrated biometal science. Vol.13, No.1 (2021). doi:10.1093/mtomcs/mfaa006 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/76302
Research Projects
Organizational Units
Authors
Journal Issue
relationships.isThesisOf
item.page.dc.title
Intracellular nickel accumulation induces apoptosis and cell cycle arrest in human astrocytic cells
item.page.dc.contributor.author
item.page.dc.description.abstract
Nickel, a heavy metal found in electronic wastes and fume from electronic cigarettes, induces neuronal cell death and is associated with neurocognitive impairment. Astrocytes are the first line of defense against nickel after entering the brain; however, the effects of nickel on astrocytes remain unknown. Herein, we investigated the effect of nickel exposure on cell survival and proliferation and the underlying mechanisms in U-87 MG human astrocytoma cells and primary human astrocytes. Intracellular nickel levels were elevated in U-87 MG cells in a dose- and time-dependent manner after exposure to nickel chloride. The median toxic concentrations of nickel in astrocytoma cells and primary human astrocytes were 600.60 and >1000 µM at 48 h post-exposure, respectively. Nickel exposure triggered apoptosis in concomitant with the decreased expression of anti-apoptotic B-cell lymphoma protein (Bcl-2) and increased caspase-3/7 activity. Nickel induced reactive oxygen species formation. Additionally, nickel suppressed astrocyte proliferation in a dose- and time-dependent manner by delaying G2 to M phase transition through the upregulation of cyclin B1 and p27 protein expression. These results indicate that nickel-induced cytotoxicity of astrocytes is mediated by the activation of apoptotic pathway and disruption of cell cycle regulation.