| Literature DB >> 30796965 |
Liping Bai1, Se Zhang2, Xiaoshuang Zhou2, Ye Li2, Jie Bai3.
Abstract
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.Entities:
Keywords: Brain-derived neurotrophic factor; Phosphatidylinositol 3-kinase; Thioredoxin-1; Tyrosine kinase B; cAMP response element-binding protein
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Year: 2019 PMID： 30796965 DOI： 10.1016/j.biochi.2019.02.011
Source DB: PubMed Journal: Biochimie ISSN： 0300-9084 Impact factor: 4.079