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B23/Nucleophosmin 促进损伤后海马体突触通路的重建。

B23/Nucleophosmin promotes reconstitution of synaptic path in hippocampus after injury.

机构信息

Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, 16419, South Korea; Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, 16419, South Korea.

Department of Medicine, Sungkyunkwan University School of Medicine, Suwon, 16419, South Korea.

出版信息

Biochem Biophys Res Commun. 2019 Jan 22;508(4):1082-1087. doi: 10.1016/j.bbrc.2018.12.036. Epub 2018 Dec 12.

DOI:10.1016/j.bbrc.2018.12.036
PMID:30553452
Abstract

B23, also known as nucleophosmin (NPM), is multifunctional protein directly implicated in cell proliferation, cell cycle progression, and cell survival. In the current study, in addition to confirming its anti-apoptotic function in neuronal survival, we demonstrated that the spatial-temporal expression profile of B23 during development of hippocampal neurons is high in the embryonic stage, down-regulated after birth, and preferentially localized at the tips of growing neuritis and branching points. Overexpression of B23 promotes axon growth with abundant branching points in growing hippocampal neurons, but depletion of B23 impairs axon growth, leading to neuronal death. Following injury to the trisynaptic path in hippocampal slice, overexpression of B23 remarkably increased the number and length of regenerative fibers in the mossy fiber path. Our study suggests that B23 expression in developing neurons is essential for neuritogenesis and axon growth and that up-regulation of B23 may be a strategy for enhancing the reconstitution of synaptic paths after injury to hippocampal synapses.

摘要

B23,也称为核仁磷酸蛋白(NPM),是一种多功能蛋白,直接参与细胞增殖、细胞周期进程和细胞存活。在本研究中,除了证实其在神经元存活中的抗凋亡功能外,我们还证明了 B23 在海马神经元发育过程中的时空表达谱在胚胎期较高,出生后下调,并且优先定位于生长轴突的末端和分支点。B23 的过表达促进了生长海马神经元中轴突的生长,并具有丰富的分支点,但 B23 的耗竭会损害轴突的生长,导致神经元死亡。在海马切片的三突触通路损伤后,B23 的过表达显著增加了苔藓纤维通路中再生纤维的数量和长度。我们的研究表明,发育中的神经元中 B23 的表达对于神经突发生和轴突生长至关重要,上调 B23 可能是增强海马突触损伤后突触通路重建的策略。

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