Knockdown of peroxiredoxin V increases glutamateinduced apoptosis in HT22 hippocampal neuron cells.
Mol Med Rep
; 17(6): 7827-7834, 2018 Jun.
Article
em En
| MEDLINE
| ID: mdl-29620243
ABSTRACT
High concentrations of glutamate may mediate neuronal cell apoptosis by increasing intracellular reactive oxygen species (ROS) levels. Peroxiredoxin V (Prx V), a member of the Prx family, serves crucial roles in protecting cells from oxidative stress. The present study investigated the regulatory effect of Prx V on glutamateinduced effects on viability and apoptosis in HT22 cells. Western blotting was used for protein expression analysis and Annexin V/PI staining and flow cytometry for determination of apoptosis. The results demonstrated that glutamate may ROSdependently increase HT22 cell apoptosis and upregulate Prx V protein levels. Furthermore, knockdown of Prx V protein expression with a lentivirus significantly enhanced HT22 cell apoptosis mediated by glutamate, which was reversed by inhibition of ROS with NacetylLcysteine. Inhibiting the extracellular signalregulated kinase (ERK) signaling pathway with PD98059, a specific inhibitor for ERK phosphorylation, markedly decreased glutamateinduced HT22 cell apoptosis in Prx V knockdown cells, indicating the potential involvement of ERK signaling in glutamateinduced HT22 cell apoptosis. In addition, an increase in nuclear apoptosisinducing factor was observed in Prx V knockdown HT22 cells following glutamate treatment, compared with mock cells, whereas no differences in Bcell lymphoma2 and cleavedcaspase3 protein expression levels were observed between mock and Prx V knockdown cells. The results of the present study indicated that Prx V may have potential as a therapeutic molecular target for glutamateinduced neuronal cell death and provide novel insight into the role of Prx V in oxidativestress induced neuronal cell death.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Apoptose
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Células Piramidais
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Ácido Glutâmico
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Peroxirredoxinas
Limite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2018
Tipo de documento:
Article