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施万细胞分化的负调控因子——周围神经治疗的新靶点?

Negative regulators of schwann cell differentiation-novel targets for peripheral nerve therapies?

机构信息

Department of Neurology, Heinrich-Heine-University of Düsseldorf, Moorenstrasse 5, Düsseldorf 40225, Germany.

出版信息

J Clin Immunol. 2013 Jan;33 Suppl 1:S18-26. doi: 10.1007/s10875-012-9786-9. Epub 2012 Sep 6.

DOI:10.1007/s10875-012-9786-9
PMID:22956147
Abstract

As myelinating glial cells of the peripheral nervous system, Schwann cells wrap around axons and thereby provide insulation, acceleration of electric signal propagation, and axonal protection and maintenance. Schwann cells are main effectors for regeneration in a variety of peripheral neuropathic conditions, including inherited, inflammatory, toxic, and diabetic neuropathies, as well as traumatic injuries to peripheral nerve fibers. Due to their high differentiation plasticity, these cells can respond to injury and disease by myelin sheath degradation, dedifferentiation into an immature Schwann cell-like phenotype, proliferation, and remyelination of sprouting axons. In doing so, they can support and promote axonal regrowth and target tissue innervation. Developmental differentiation as well as regenerative de- and redifferentiation are tightly controlled by a balance of positive and negative regulators of Schwann cell maturation. Since misregulated expression of such negative regulators is potentially involved in inefficient or failed regeneration, we will provide an overview about recent work revealing the complex interactions between extrinsic and intrinsic signals in the inhibition of Schwann cell differentiation.

摘要

作为周围神经系统的髓鞘形成胶质细胞,施万细胞包裹在轴突周围,从而提供绝缘、加速电信号的传播,并保护和维持轴突。施万细胞是多种周围神经病变情况下再生的主要效应物,包括遗传性、炎症性、毒性和糖尿病性神经病,以及周围神经纤维的创伤性损伤。由于其高度分化的可塑性,这些细胞可以通过髓鞘降解、去分化为未成熟的施万细胞样表型、增殖和发芽轴突的再髓鞘化来响应损伤和疾病。这样,它们可以支持和促进轴突的再生和靶组织的神经支配。发育分化以及再生的去分化和再分化受到施万细胞成熟的正、负调节因子平衡的严格控制。由于这些负调节因子的表达失调可能与再生效率低下或失败有关,因此我们将概述最近的工作,揭示外在和内在信号在抑制施万细胞分化中的复杂相互作用。

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Negative regulators of schwann cell differentiation-novel targets for peripheral nerve therapies?施万细胞分化的负调控因子——周围神经治疗的新靶点?
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2
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本文引用的文献

1
Histone methyltransferase enhancer of zeste homolog 2 regulates Schwann cell differentiation.EZH2 调控施万细胞分化。
Glia. 2012 Nov;60(11):1696-708. doi: 10.1002/glia.22388. Epub 2012 Jul 20.
2
c-Jun in Schwann cells promotes axonal regeneration and motoneuron survival via paracrine signaling.施万细胞中的 c-Jun 通过旁分泌信号促进轴突再生和运动神经元存活。
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Regulation of Schwann cell differentiation and proliferation by the Pax-3 transcription factor.
糖尿病伤口代谢异常的机制与治疗机遇:一篇综述
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Immortalized Schwann cell lines as useful tools for pathogenesis-based therapeutic approaches to diabetic peripheral neuropathy.永生化雪旺细胞系作为基于发病机制的糖尿病周围神经病变治疗方法的有用工具。
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The dynamic changes of main cell types in the microenvironment of sciatic nerves following sciatic nerve injury and the influence of let-7 on their distribution.坐骨神经损伤后坐骨神经微环境中主要细胞类型的动态变化以及let-7对其分布的影响。
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Upregulation of lncRNA147410.3 in the Brain of Mice With Chronic Infection Promoted Microglia Apoptosis by Regulating Hoxb3.慢性感染小鼠大脑中lncRNA147410.3的上调通过调控Hoxb3促进小胶质细胞凋亡。
Front Cell Neurosci. 2021 May 18;15:648047. doi: 10.3389/fncel.2021.648047. eCollection 2021.
7
CXCL12 induces migration of Schwann cells via p38 MAPK and autocrine of CXCL12 by the CXCR4 receptor.CXCL12通过p38丝裂原活化蛋白激酶诱导雪旺细胞迁移,并通过CXCR4受体自分泌CXCL12。
Int J Clin Exp Pathol. 2018 Jun 1;11(6):3119-3125. eCollection 2018.
8
Myelination key factor krox-20 is downregulated in Schwann cells and murine sciatic nerves infected by Mycobacterium leprae.髓鞘形成关键因子 krox-20 在麻风分枝杆菌感染的雪旺细胞和小鼠坐骨神经中表达下调。
Int J Exp Pathol. 2019 Apr;100(2):83-93. doi: 10.1111/iep.12309. Epub 2019 May 14.
9
Preventive action of benztropine on platinum-induced peripheral neuropathies and tumor growth.苯海索对铂诱导的周围神经病变和肿瘤生长的预防作用。
Acta Neuropathol Commun. 2019 Jan 18;7(1):9. doi: 10.1186/s40478-019-0657-y.
10
Increased levels of miR-3099 induced by peripheral nerve injury promote Schwann cell proliferation and migration.外周神经损伤诱导的miR-3099水平升高促进雪旺细胞增殖和迁移。
Neural Regen Res. 2019 Mar;14(3):525-531. doi: 10.4103/1673-5374.245478.
Pax-3 转录因子对施万细胞分化和增殖的调控。
Glia. 2012 Sep;60(9):1269-78. doi: 10.1002/glia.22346. Epub 2012 Apr 24.
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Genetic disruption of Pten in a novel mouse model of tomaculous neuropathy.新型巨轴索神经病小鼠模型中 Pten 的基因缺失。
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A central role for the ERK-signaling pathway in controlling Schwann cell plasticity and peripheral nerve regeneration in vivo.ERK 信号通路在体内控制施万细胞可塑性和周围神经再生中的核心作用。
Neuron. 2012 Feb 23;73(4):729-42. doi: 10.1016/j.neuron.2011.11.031.
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Nuclear factor-κB activation in Schwann cells regulates regeneration and remyelination.施旺细胞中核因子-κB 的激活调节再生和髓鞘形成。
Glia. 2012 Apr;60(4):639-50. doi: 10.1002/glia.22297. Epub 2012 Jan 24.
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c-Jun expression in human neuropathies: a pilot study.c-Jun 在人类神经病变中的表达:一项初步研究。
J Peripher Nerv Syst. 2011 Dec;16(4):295-303. doi: 10.1111/j.1529-8027.2011.00360.x.
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The atypical Guanine-nucleotide exchange factor, dock7, negatively regulates schwann cell differentiation and myelination.非典型鸟嘌呤核苷酸交换因子 Dock7 负调控许旺细胞分化和髓鞘形成。
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Retinoic acid reduces chemotherapy-induced neuropathy in an animal model and patients with lung cancer.维甲酸可减少动物模型和肺癌患者的化疗引起的周围神经病。
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Interplay between LXR and Wnt/β-catenin signaling in the negative regulation of peripheral myelin genes by oxysterols.氧化固醇通过 LXR 和 Wnt/β-连环蛋白信号通路负调控外周髓鞘基因的相互作用。
J Neurosci. 2011 Jun 29;31(26):9620-9. doi: 10.1523/JNEUROSCI.0761-11.2011.