Tamoxifen Induces Apoptosis of Mouse Microglia Cell Line BV-2 Cells via both Mitochondrial and Death Receptor Pathways

Little is known about whether tamoxifen (TAM) can affect resting state microglia apoptosis and about the cellular mechanism that may account for this. To explore this question, we incubated the microglia cell line BV-2 cells with TAM at different concentrations. Cell viability was assessed by the MT...

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Bibliographic Details
Published in:Journal of Huazhong University of Science and Technology. Medical sciences 2012-04, Vol.32 (2), p.221-226
Main Author: 李正伟 陈劲草 雷霆 张华楸
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Bax protein
Bcl-2 protein
CD95 antigen
Cell Line
Cell Survival - drug effects
Cell Survival - physiology
cells
death
death receptors
Dose-Response Relationship, Drug
Fas antigen
Flow cytometry
Medicine
Medicine & Public Health
Membrane potential
Mice
Microglia
Microglia - drug effects
Microglia - physiology
Microglia - ultrastructure
Mitochondria
Mitochondria - drug effects
Mitochondria - physiology
Mitochondria - ultrastructure
receptor
Receptors, Death Domain - metabolism
Signal Transduction - drug effects
Signal Transduction - physiology
Tamoxifen
Tamoxifen - pharmacology
Western blotting
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Summary:Little is known about whether tamoxifen (TAM) can affect resting state microglia apoptosis and about the cellular mechanism that may account for this. To explore this question, we incubated the microglia cell line BV-2 cells with TAM at different concentrations. Cell viability was assessed by the MTT assay, and flow cytometric analysis was performed to detect the cell apoptosis rate. Furthermore, mitochondrial membrane potential (Δψm) was tested by flow cytometry, and Bax, Bcl-2, Fas, and Fas-L expression was detected by Western blot. The results demonstrated that TAM decreased cell viability and induced apoptosis of BV-2 cells in a concentration- and time-dependent manner. In addition, disrup-tion of Δψm was followed by up-regulated expression of pro-apoptotic Bax, Fas and Fas-L, and down-regulated expression of anti-apoptotic Bcl-2. These results indicate that TAM may induce apop-tosis of BV-2 cells through both mitochondria- and death receptor-mediated pathways.
ISSN:1672-0733
1993-1352
DOI:10.1007/s11596-012-0039-1