ORC ID , Wei-Chun Guo PhD 1, Zhao-Hui Zhang2">
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RESEARCH ARTICLE
Year : 2020  |  Volume : 15  |  Issue : 6  |  Page : 1066-1070

Proprotein convertase 1/3-mediated down-regulation of brain-derived neurotrophic factor in cortical neurons induced by oxygen-glucose deprivation


1 Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China
2 Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China

Correspondence Address:
Wei-Chun Guo
Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, Hubei Province
China
Yan Chen
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province
China
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Source of Support: This study was supported by the National Nature Science Foundation of China, No. 81501053 (to YC), Conflict of Interest: None


DOI: 10.4103/1673-5374.270314

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Brain-derived neurotrophic factor (BDNF) has robust effects on synaptogenesis, neuronal differentiation and synaptic transmission and plasticity. The maturation of BDNF is a complex process. Proprotein convertase 1/3 (PC1/3) has a key role in the cleavage of protein precursors that are directed to regulated secretory pathways; however, it is not clear whether PC1/3 mediates the change in BDNF levels caused by ischemia. To clarify the role of PC1/3 in BDNF maturation in ischemic cortical neurons, primary cortical neurons from fetal rats were cultured in a humidified environment of 95% N2 and 5% CO2 in a glucose-free Dulbecco’s modified Eagle’s medium at 37°C for 3 hours. Enzyme-linked immunosorbent assays and western blotting showed that after oxygen-glucose deprivation, the secreted and intracellular levels of BDNF were significantly reduced and the intracellular level of PC1/3 was decreased. Transient transfection of cortical neurons with a PC1/3 overexpression plasmid followed by oxygen-glucose deprivation resulted in increased PC1/3 levels and increased BDNF levels. When levels of the BDNF precursor protein were reduced, the concentration of BDNF in the culture medium was increased. These results indicate that PC1/3 cleavage of BDNF is critical for the conversion of pro-BDNF in rat cortical neurons during ischemia. The study was approved by the Animal Ethics Committee of Wuhan University School of Basic Medical Sciences.


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