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以自噬非依赖的方式诱导 PC12 和 C17.2 细胞的神经突生长和分化。

Induces Neurite Outgrowth and Differentiation in an Autophagy-Independent Manner in PC12 and C17.2 Cells.

机构信息

Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.

Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.

出版信息

Front Cell Infect Microbiol. 2018 Jun 19;8:201. doi: 10.3389/fcimb.2018.00201. eCollection 2018.

DOI:10.3389/fcimb.2018.00201
PMID:29988402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6024096/
Abstract

Both pathogenic and non-pathogenic can induce the differentiation of immune cells into dendritic cells (DC) or DC-like cells. In addition, pathogenic is found to stimulate cell differentiation in the nerves system. Whether non-pathogenic interacts with nerve cells remains unknown. In this study, we found that co-incubation with fast-growing induced neuron-like morphological changes of PC12 and C17.2 cells. Moreover, the culture supernatant which was ultrafiltrated through a membrane with a 10 kDa cut-off, induced neurite outgrowth and differentiation in an autophagy-independent pathway in PC12 and C17.2 cells. Further analysis showed that IFN-γ production and activation of the PI3K-Akt signaling pathway were involved in the neural differentiation. In conclusion, our finding demonstrated that non-pathogenic was able to promote neuronal differentiation by its extracellular proteins, which might provide a novel therapeutic strategy for the treatment of neurodegenerative disorders.

摘要

无论是病原性还是非病原性的,都可以诱导免疫细胞分化为树突状细胞(DC)或类似 DC 的细胞。此外,已发现病原性能够刺激神经系统中的细胞分化。而非病原性是否与神经细胞相互作用尚不清楚。在本研究中,我们发现与快速生长的共孵育诱导 PC12 和 C17.2 细胞产生神经元样形态变化。此外,通过 10 kDa 截止值的膜超滤的培养上清液,在 PC12 和 C17.2 细胞中诱导了独立于自噬的轴突生长和分化。进一步分析表明,IFN-γ的产生和 PI3K-Akt 信号通路的激活参与了神经分化。总之,我们的发现表明,非病原性可以通过其细胞外蛋白促进神经元分化,这可能为治疗神经退行性疾病提供一种新的治疗策略。

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