Brain-derived neurotrophic factor induces thioredoxin-1 expression through TrkB/Akt/CREB pathway in SH-SY5Y cells

被引:33
作者
Bai, Liping [1 ,2 ]
Zhang, Se [2 ]
Zhou, Xiaoshuang [2 ]
Li, Ye [2 ]
Bai, Jie [2 ]
机构
[1] Kunming Univ Sci & Technol, Fac Environm Sci & Engn, Kunming 650500, Yunnan, Peoples R China
[2] Kunming Univ Sci & Technol, Lab Mol Neurobiol, Med Fac, Kunming 650500, Yunnan, Peoples R China
基金
中国国家自然科学基金;
关键词
Brain-derived neurotrophic factor; Thioredoxin-1; Tyrosine kinase B; Phosphatidylinositol; 3-kinase; cAMP response element-binding protein; OXIDATIVE STRESS; CREB; MEMORY; SIGNAL; BDNF; TRKB; INVOLVEMENT; ACTIVATION; PLASTICITY; KINASE;
D O I
10.1016/j.biochi.2019.02.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Brain-derived neurotrophic factor (BDNF) is one of the neurotrophic factors that are vital to the survival and proliferation of neuron. Thioredoxin-1 (Trx-1) is a redox regulating protein and plays various roles in regulating transcript factors and inhibiting apoptosis. It has been reported that Trx-1 is required for nerve growth factor-mediated signal transduction and neurite outgrowth, and is involved in synaptic protein expression induced by BDNF. However, the molecular mechanism on BDNF inducing Trx-1 expression has not been fully verified. The present study investigated the expression of Trx-1 after treatment with BDNF in SH-SY5Y cells. We first demonstrated that cell viability and the expression of Trx-1 were increased by BDNF in SH-SY5Y cells, which were inhibited by the tyrosine kinase B (TrkB) inhibitor, K252a, and the phosphatidylinositol 3-kinase (PI3-K) inhibitor, LY294002. Moreover, BDNF increased the activity of cAMP response element-binding protein (CREB) through TrkB/PI3-K/Akt pathway. Whereas the expression of Trx-1 induced by BDNF was suppressed by CREB siRNA. Thus, our data suggest that BDNF induces the expression of Trx-1 through the TrkB/Akt/CREB pathway. (C) 2019 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved.
引用
收藏
页码:55 / 60
页数:6
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