脑源性神经营养因子通过 TrkB/Akt/CREB 通路诱导 SH-SY5Y 细胞中硫氧还蛋白-1 的表达。
Brain-derived neurotrophic factor induces thioredoxin-1 expression through TrkB/Akt/CREB pathway in SH-SY5Y cells.
机构信息
Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming, 650500, China; Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming, 650500, China.
Laboratory of Molecular Neurobiology, Medical Faculty, Kunming University of Science and Technology, Kunming, 650500, China.
出版信息
Biochimie. 2019 May;160:55-60. doi: 10.1016/j.biochi.2019.02.011. Epub 2019 Feb 20.
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.
脑源性神经营养因子（BDNF）是对神经元的存活和增殖至关重要的神经营养因子之一。硫氧还蛋白-1（Trx-1）是一种氧化还原调节蛋白，在调节转录因子和抑制细胞凋亡方面发挥着各种作用。据报道，Trx-1 是神经营养因子介导的信号转导和神经突生长所必需的，并且参与 BDNF 诱导的突触蛋白表达。然而，BDNF 诱导 Trx-1 表达的分子机制尚未完全验证。本研究探讨了 BDNF 处理后 SH-SY5Y 细胞中 Trx-1 的表达。我们首先证明，BDNF 可增加 SH-SY5Y 细胞的细胞活力和 Trx-1 的表达，而酪氨酸激酶 B（TrkB）抑制剂 K252a 和磷脂酰肌醇 3-激酶（PI3-K）抑制剂 LY294002 可抑制其表达。此外，BDNF 通过 TrkB/PI3-K/Akt 通路增加 cAMP 反应元件结合蛋白（CREB）的活性。而 BDNF 诱导的 Trx-1 表达则被 CREB siRNA 抑制。因此，我们的数据表明，BDNF 通过 TrkB/Akt/CREB 通路诱导 Trx-1 的表达。
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