树突状细胞通过NT-3/TrkC信号通路调控神经干细胞存活的体外研究

王钟; 陈太邦; 王永飞; 郭乔楠; 赵建华

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树突状细胞通过NT-3/TrkC信号通路调控神经干细胞存活的体外研究

论著 | 更新时间：2026-01-09

- 树突状细胞通过NT-3/TrkC信号通路调控神经干细胞存活的体外研究
- Dendritic cell-induced neural stem cell survival via NT-3/TrkC signaling pathway
- 陆军军医大学学报 2013年35卷第12期页码：1188-1191
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  中图分类号： R322.8;R329-33;R329.26
- 纸质出版：2013
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王钟,陈太邦,王永飞,郭乔楠,赵建华.树突状细胞通过NT-3/TrkC信号通路调控神经干细胞存活的体外研究[J].陆军军医大学学报(原第三军医大学学报),2013,35(12):1188-1191.

　Wang Zhong,Chen Taibang,Wang Yongfei,Guo Qiaonan,Zhao Jianhua.Dendritic cell-induced neural stem cell survival via NT-3/TrkC signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(12):1188-1191.
王钟,陈太邦,王永飞,郭乔楠,赵建华.树突状细胞通过NT-3/TrkC信号通路调控神经干细胞存活的体外研究[J].陆军军医大学学报(原第三军医大学学报),2013,35(12):1188-1191. DOI：

　Wang Zhong,Chen Taibang,Wang Yongfei,Guo Qiaonan,Zhao Jianhua.Dendritic cell-induced neural stem cell survival via NT-3/TrkC signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(12):1188-1191. DOI：

摘要

目的研究共培养状态下树突状细胞(dendritic cell

DC)对神经干细胞（neural stem cell

NSC）存活的影响及其作用机制。方法体外分离、纯化SD大鼠原代DC和NSC，将二者用Transwell技术共培养，用NT-3特异性抗体中和NT-3的表达；然后采用qRT-PCR方法检测DC中神经营养素-3（neurotrophin-3

NT-3）的mRNA水平，流式细胞术检测NSC凋亡；同时用免疫荧光、Western blot技术确定NSC表面NT-3特异性受体Trk C的表达。结果与DC单独培养组相比，共培养体系中，DC表达NT-3水平显著性增强（

0.05)；同时共培养能显著增加NSC存活，该效应能被NT-3特异性中和性抗体阻断；共培养能够增加NSC中NT-3特异性受体TrkC表达（

0.05)，并上调TrkC磷酸化水平，而NT-3特异性抗体能够抑制TrkC表达和磷酸化上调（

0.05)。结论 DC和NSC共培养能够增加DC中NT-3表达，高表达的NT-3则通过NSC膜上的TrkC受体促进NSC的存活。

Abstract

Objective To study the effect of dendritic cell (DC) on neural stem cell (NSC) survival when they were cocultured in vitro. Methods Primary DC and NSC isolated and purified from SD rats were cocultured by Transwell technique in vitro. The expression of neurotrophin-3 (NT-3) mRNA in DC was determined by qRT-PCR

and the apoptotic ratio of NSC was detected with flow cytometry. In addition

the expression of NT-3 specific receptor tropomyosin receptor kinase C (TrkC) in NSC was detected with immuno flourescence and Western blotting. Results

Compared with simple DC group

the expression of NT-3 significantly increased in the DC cocultured with NSC (

0.05). The survival of NSC markedly increased and the effect was selectively blocked by a NT-3 specific neutralizing antibody. In addition

the levels of expression and phosphorylation of NT-3 specific receptor TrkC significantly increased in NSC (

0.05)

and the increase could also be inhibited by the NT-3 specific neutralizing antibody. Conclusion Coculture of DC and NSC upregulates the expression of NT-3 in DC and promotes the survival of NSC in a NT-3/TrkC-dependent manner.

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