Activating Transcription Factor 4 Modulates BDNF Release from Microglial Cells

Pathogenic pain is a common sign of many diseases. The mechanism is unclear. Activating transcription factor 4 (ATF4) plays a critical role in cell activation. Brain-derived neurotrophic factor (BDNF) is an important molecule in pathogenic pain. This study aims to investigate the role of ATF4 in ind...

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Bibliographic Details
Published in:Journal of molecular neuroscience 2014-02, Vol.52 (2), p.225-230
Main Authors: Sun, Pengling, Li, Xiangnan, Chen, Chengwen, Chen, Qianbo, Ouyang, Qing, Liu, Fangting, Xiang, Zhenghua, Yuan, Hongbin
Format: Article
Language:English
Subjects:
Activating Transcription Factor 4 - genetics
Activating Transcription Factor 4 - metabolism
Anesthesiology
Animals
Antibodies
Apoptosis
Biomedical and Life Sciences
Biomedicine
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - genetics
Brain-Derived Neurotrophic Factor - metabolism
Cell Biology
Cell culture
Cell Line
Enzymes
Flow cytometry
Hospitals
Hypoxia
Mice
Microglia - metabolism
Microglia - physiology
Neurobiology
Neurochemistry
Neurology
Neurosciences
Pain
Pathogenesis
Proteomics
Reagents
Receptor, PAR-2 - genetics
Receptor, PAR-2 - metabolism
Transcription factors
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Summary:Pathogenic pain is a common sign of many diseases. The mechanism is unclear. Activating transcription factor 4 (ATF4) plays a critical role in cell activation. Brain-derived neurotrophic factor (BDNF) is an important molecule in pathogenic pain. This study aims to investigate the role of ATF4 in inducing BDNF release from microglial cells. In this study, mouse microglial cells were cultured. The levels of BDNF in the culture medium were determined by enzyme-linked immunosorbent assay. Overexpression of ATF4 in microglial cells was performed by gene transfection. The apoptosis of microglial cells was assessed by flow cytometry. The results showed that microglial cells expressed ATF4 and protease-activated receptor-2 (PAR2). BDNF was detectable in the culture medium of microglial cells, which was significantly increased in the ATF4-overexpressing microglial cells. The ATF4-overexpressing microglial cells showed a high frequency of apoptotic cells, which could be inhibited by exposure to the PAR2 agonist tryptase in the culture. The tryptase-treated ATF4-overexpressing microglial cells kept higher secretion of BDNF. We conclude that the activation of ATF4 can increase BDNF release from microglial cells.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-013-0126-1