Collagen Nanofibers Facilitated Presynaptic Maturation in Differentiated Neurons from Spinal-Cord-Derived Neural Stem Cells through MAPK/ERK1/2-Synapsin I Signaling Pathway

Collagen Nanofibers Facilitated Presynaptic Maturation in Differentiated Neurons from Spinal-Cord-Derived Neural Stem Cells through MAPK/ERK1/2-Synapsin I Signaling Pathway
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胶原纳米纤维通过 MAPK/ERK1/2-Synapsin I 信号通路促进脊髓源性神经干细胞分化神经元的突触前成熟。

DOI:
10.1021/bm500321h
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发表时间:
2014-07-01
期刊:
影响因子:
6.2
通讯作者:
Wang, Yansong
Wang, Yansong
中科院分区:
化学2区
文献类型:
--
作者:
Yin, Yanling;Huang, Peng;Wang, Yansong

文献摘要

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神经干细胞(NSCs)被认为是脑和脊髓损伤后重建和再生的潜在细胞疗法。在这项研究中,我们研究了纳米纤维支架在nscs来源的神经元形成中的作用。将脊髓源性NSCs分化成神经元,体外培养10 ~ 14 d后,采用全细胞膜片钳法记录微型兴奋性突触后电流(mEPSCs)。结果发现,在随机定向和排列的胶原纳米纤维支架上培养的分化神经元中,mEPSCs的频率高于胶原包被对照组,并且可以被ERK抑制剂(PD98059)抑制,这表明胶原纳米纤维通过MAPK/ERK1/2途径影响突触前位点的成熟。此外,两种胶原纳米纤维都增加了Synapsin I的磷酸化,促进了p-ERK1/2和p-Synapsin I的相互作用。这些结果表明,胶原纳米纤维支架通过ERK1/2-Synapsin I信号通路促进了突触前成熟。
Neural stem cells (NSCs) are deemed to be a potential cell therapy for brain and spinal cord reconstruction and regeneration following injury. In this study, we investigated the role of nanofibrous scaffolds on NSCs-derived neurons in the formation of neural networks. Miniature excitatory postsynaptic currents (mEPSCs) were recorded using the whole-cell patch clamp recording method after the spinal cord-derived NSCs were differentiated into neurons and cultured in vitro for 10-14 days. It was observed that the frequency of mEPSCs in the differentiated neurons cultured on both randomly oriented and aligned collagen nanofibrous scaffolds was higher than that on the collagen-coated control and can be inhibited by an ERK inhibitor (PD98059), indicating that the collagen nanofibers affected the maturation of the synapses from presynaptic sites via the MAPK/ERK1/2 pathway. In addition, both of the collagen nanofibers increased the phosphorylation of Synapsin I and facilitated the interaction of p-ERK1/2 and p-Synapsin I. All these results suggested that the collagen nanofibrous scaffolds contributed to the presynaptic maturation via the ERK1/2-Synapsin I signaling pathway.