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脉冲电磁场通过新生大鼠背根神经节神经元中的L型电压门控钙通道和依赖细胞外信号调节激酶的信号通路增强脑源性神经营养因子的表达。

Pulsed electromagnetic field enhances brain-derived neurotrophic factor expression through L-type voltage-gated calcium channel- and Erk-dependent signaling pathways in neonatal rat dorsal root ganglion neurons.

作者信息

Li Yuan, Yan Xiaodong, Liu Juanfang, Li Ling, Hu Xinghua, Sun Honghui, Tian Jing

机构信息

Second Clinical Medical College, Southern Medical University, Guangzhou 510280, PR China.

Department of Orthopaedics, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, PR China.

出版信息

Neurochem Int. 2014 Sep;75:96-104. doi: 10.1016/j.neuint.2014.06.004. Epub 2014 Jun 14.

Abstract

Although pulsed electromagnetic field (PEMF) exposure has been reported to promote neuronal differentiation, the mechanism is still unclear. Here, we aimed to examine the effects of PEMF exposure on brain-derived neurotrophic factor (Bdnf) mRNA expression and the correlation between the intracellular free calcium concentration ([Ca(2+)]i) and Bdnf mRNA expression in cultured dorsal root ganglion neurons (DRGNs). Exposure to 50Hz and 1mT PEMF for 2h increased the level of [Ca(2+)]i and Bdnf mRNA expression, which was found to be mediated by increased [Ca(2+)]i from Ca(2+) influx through L-type voltage-gated calcium channels (VGCCs). However, calcium mobilization was not involved in the increased [Ca(2+)]i and BDNF expression, indicating that calcium influx was one of the key factors responding to PEMF exposure. Moreover, PD098059, an extracellular signal-regulated kinase (Erk) inhibitor, strongly inhibited PEMF-dependant Erk1/2 activation and BDNF expression, indicating that Erk activation is required for PEMF-induced upregulation of BDNF expression. These findings indicated that PEMF exposure increased BDNF expression in DRGNs by activating Ca(2+)- and Erk-dependent signaling pathways.

摘要

尽管有报道称脉冲电磁场(PEMF)暴露可促进神经元分化,但其机制仍不清楚。在此,我们旨在研究PEMF暴露对培养的背根神经节神经元(DRGNs)中脑源性神经营养因子(Bdnf)mRNA表达的影响,以及细胞内游离钙浓度([Ca(2+)]i)与Bdnf mRNA表达之间的相关性。暴露于50Hz和1mT的PEMF 2小时可增加[Ca(2+)]i水平和Bdnf mRNA表达,发现这是由通过L型电压门控钙通道(VGCCs)的Ca(2+)内流导致的[Ca(2+)]i增加所介导的。然而,钙动员并不参与[Ca(2+)]i和BDNF表达的增加,表明钙内流是对PEMF暴露作出反应的关键因素之一。此外,细胞外信号调节激酶(Erk)抑制剂PD098059强烈抑制PEMF依赖的Erk1/2激活和BDNF表达,表明Erk激活是PEMF诱导BDNF表达上调所必需的。这些发现表明,PEMF暴露通过激活Ca(2+)和Erk依赖的信号通路增加了DRGNs中BDNF的表达。

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