The neuroprotective role of brain-derived neurotrophic factor for embryonic rat cortical neurons against hypoxia via CREB phosphorylation.
- Author:
Xiaoli LUO
1
;
Hui ZHOU
;
Xiaomei SUN
;
Shengfu LI
;
Dezhi MU
;
Meng MAO
Author Information
1. Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain-Derived Neurotrophic Factor;
chemistry;
pharmacology;
Cell Hypoxia;
Cells, Cultured;
Cerebral Cortex;
cytology;
Cyclic AMP Response Element-Binding Protein;
chemistry;
Embryo, Mammalian;
Neurons;
cytology;
Neuroprotective Agents;
chemistry;
pharmacology;
Phosphorylation;
Rats
- From:
Journal of Biomedical Engineering
2008;25(6):1377-1380
- CountryChina
- Language:Chinese
-
Abstract:
Transcription factor cyclic AMP response element-binding protein (CREB) in embryonic cortical neurons is an important modulator of Brain-derived neurotrophic factor (BDNF) induced gene expression. Meanwhile, our early researches have indicated that BDNF possesses neuroprotective role for hypoxic neurons against hypoxia. In order todisclose whether the neuroprotective role of BDNF for embryonic rat cortical neurons against hypoxia is fulfilled via nucleoprotein CREB phosphorylation, we used western blotting method to detect the expression of CREB and phosphorylated CREB in experimental groups (with BDNF) and hypoxic control group (without BDNF) with the time changes of exposure to hypoxia. Results indicated that hypoxia and BDNF both could induce phosphorylation of CREB in embryonic cortical neurons. Phosphorylation of CREB in experimental group (with BDNF) was much higher than that in hypoxic control group at the same time points (P<0.01). The expression of phosphorylated CREB reached the highest level at the first hour after being exposed to hypoxia in experimental groups, then phosphorylated CREB decreased slowly and remained at the level for much longer time in experimental groups than in control group. The total amount of CREB in embryonic cortical neurons at the first 0-3 hours after being exposed to hypoxia in experimental groups were the same as that in hypoxic control group. CREB decreased more quickly in hypoxic control group at 5-6 hours after hypoxia. This in vitro research demonstrates that BDNF plays its neuroprotective role for embryonic rat cortical neurons against hypoxia via CREB phosphorylation.
