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本文引用的文献

1
The roles of neuron-NG2 glia synapses in promoting oligodendrocyte development and remyelination.神经元-NG2 胶质细胞突触在促进少突胶质细胞发育和髓鞘修复中的作用。
Cell Tissue Res. 2020 Jul;381(1):43-53. doi: 10.1007/s00441-020-03195-9. Epub 2020 Mar 31.
2
Activation of the Notch Signaling Pathway and Cellular Localization of Notch Signaling Molecules in the Spinal Cord of SOD1-G93A ALS Model Mice.SOD1-G93A肌萎缩侧索硬化症模型小鼠脊髓中Notch信号通路的激活及Notch信号分子的细胞定位
Neuroscience. 2020 Apr 15;432:84-93. doi: 10.1016/j.neuroscience.2020.02.034. Epub 2020 Feb 28.
3
GDNF rescues the fate of neural progenitor grafts by attenuating Notch signals in the injured spinal cord in rodents.GDNF 通过减弱啮齿动物损伤脊髓中的 Notch 信号挽救神经祖细胞移植物的命运。
Sci Transl Med. 2020 Jan 8;12(525). doi: 10.1126/scitranslmed.aau3538.
4
Sox17 Regulates a Program of Oligodendrocyte Progenitor Cell Expansion and Differentiation during Development and Repair.Sox17 调控发育和修复过程中少突胶质前体细胞的扩增和分化。
Cell Rep. 2019 Dec 3;29(10):3173-3186.e7. doi: 10.1016/j.celrep.2019.10.121.
5
CNS myelin protein 36K regulates oligodendrocyte differentiation through Notch.中枢神经系统髓鞘蛋白 36K 通过 Notch 调控少突胶质细胞分化。
Glia. 2020 Mar;68(3):509-527. doi: 10.1002/glia.23732. Epub 2019 Nov 8.
6
Blocking Notch signal pathway suppresses the activation of neurotoxic A1 astrocytes after spinal cord injury.阻断 Notch 信号通路可抑制脊髓损伤后神经毒性 A1 星形胶质细胞的激活。
Cell Cycle. 2019 Nov;18(21):3010-3029. doi: 10.1080/15384101.2019.1667189. Epub 2019 Sep 18.
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Demyelination-remyelination in the Central Nervous System: Ligand-dependent Participation of the Notch Signaling Pathway.中枢神经系统中的脱髓鞘-再髓鞘化:Notch信号通路的配体依赖性参与
Toxicol Sci. 2019 Sep 1;171(1):172-192. doi: 10.1093/toxsci/kfz130.
8
MFG-E8 reverses microglial-induced neurotoxic astrocyte (A1) via NF-κB and PI3K-Akt pathways.MFG-E8 通过 NF-κB 和 PI3K-Akt 通路逆转小胶质细胞诱导的神经毒性星形胶质细胞(A1)。
J Cell Physiol. 2018 Jan;234(1):904-914. doi: 10.1002/jcp.26918. Epub 2018 Aug 4.
9
Effect of Notch1 gene on remyelination in multiple sclerosis in mouse models of acute demyelination.Notch1 基因对急性脱髓鞘小鼠模型多发性硬化症髓鞘修复的影响。
J Cell Biochem. 2018 Nov;119(11):9284-9294. doi: 10.1002/jcb.27197. Epub 2018 Jul 16.
10
Astrocyte-derived Jagged-1 mitigates deleterious Notch signaling in amyotrophic lateral sclerosis.星形胶质细胞衍生的 Jagged-1 减轻肌萎缩侧索硬化症中的有害 Notch 信号传导。
Neurobiol Dis. 2018 Nov;119:26-40. doi: 10.1016/j.nbd.2018.07.012. Epub 2018 Jul 26.

Notch 信号通路调控脱髓鞘疾病中 NG2 细胞向少突胶质细胞的分化。

The Notch Signaling Pathway Regulates Differentiation of NG2 Cells into Oligodendrocytes in Demyelinating Diseases.

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, No. 17 Yongwai Zheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.

出版信息

Cell Mol Neurobiol. 2022 Oct;42(7):1-11. doi: 10.1007/s10571-021-01089-0. Epub 2021 Apr 7.

DOI:10.1007/s10571-021-01089-0
PMID:33826017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11421596/
Abstract

NG2 cells are highly proliferative glial cells that can self-renew or differentiate into oligodendrocytes, promoting remyelination. Following demyelination, the proliferative and differentiation potentials of NG2 cells increase rapidly, enhancing their differentiation into functional myelinating cells. Levels of the transcription factors Olig1 and Olig2 increase during the differentiation of NG2 cells and play important roles in the development and repair of oligodendrocytes. However, the ability to generate new oligodendrocytes is hampered by injury-related factors (e.g., myelin fragments, Wnt and Notch signaling components), leading to failed differentiation and maturation of NG2 cells into oligodendrocytes. Here, we review Notch signaling as a negative regulator of oligodendrocyte differentiation and discuss the extracellular ligands, intracellular pathways, and key transcription factors involved.

摘要

NG2 细胞是高度增殖的神经胶质细胞,能够自我更新或分化为少突胶质细胞,促进髓鞘再生。脱髓鞘后,NG2 细胞的增殖和分化潜能迅速增加,促进其分化为具有功能的髓鞘形成细胞。转录因子 Olig1 和 Olig2 的水平在 NG2 细胞的分化过程中增加,在少突胶质细胞的发育和修复中发挥重要作用。然而,新的少突胶质细胞的产生能力受到损伤相关因子(如髓鞘碎片、Wnt 和 Notch 信号成分)的阻碍,导致 NG2 细胞分化为少突胶质细胞的失败和成熟。在这里,我们将 Notch 信号作为少突胶质细胞分化的负调节剂进行综述,并讨论涉及的细胞外配体、细胞内途径和关键转录因子。