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少突胶质细胞是中枢神经系统中形成髓鞘的高度特化的胶质细胞,由少突胶质前体细胞分化而来。长期以来,围绕少突胶质谱系细胞开展的研究主要集中在少突胶质细胞发育、髓鞘形成以及少突胶质谱系细胞在神经系统疾病中的作用等。新兴的单细胞转录组测序技术可以在转录组层面鉴定出特定类型细胞,为少突胶质谱系细胞的研究提供助力。本综述主要关注常见单细胞测序技术的发展以及它们在少突胶质细胞功能异质性和神经系统疾病研究中的应用,并对已取得的成果进行总结阐述,为单细胞测序技术在中枢神经系统疾病中少突胶质谱系细胞相关研究的应用和开发提供思路和参考。 相似文献
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《生命科学研究》2017,(6):534-541
少突胶质细胞(oligodendrocytes,OLs)在脊椎动物中枢神经系统(central nervous system,CNS)中负责形成包裹神经元轴突的髓鞘,保证神经冲动沿轴突的快速传导,并为其提供营养支持。OLs发育异常及损伤会导致严重的神经系统疾病,比如脑白质营养不良(leukodystrophy)、多发性硬化症(multiple sclerosis,MS)等。少突胶质细胞前体细胞(oligodendrocyte progenitor cells,OPCs)在胚胎期由神经前体细胞(neural progenitor cells,NPCs)产生,该过程受到一系列细胞内外因素的调控,对这一问题的研究也是神经系统研究的重要内容。现主要基于遗传学结果,简述关于OPCs产生的调控机制的最新研究进展。 相似文献
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胶质细胞生长因子的研究进展 总被引:4,自引:0,他引:4
胶质细胞生长因子(glial growth factor,GGF)是neuregulin基因的产物。GGF与erbB受体的异二聚体或同二聚体结合,催化多肽链中的酪氨酸磷酸化,激活下游信号分子而发挥其生理作用。GGF及其受体在发育及成熟神经系统中广泛分布。GGF限定神经嵴细胞,使其向雪旺氏细胞分化,并在雷旺氏细胞发育过程中发挥重要作用。GGF能够刺激少突胶质细胞前体细胞、少突胶质细胞和星形胶质细胞增殖,抑制少突胶质细胞前体细胞分化成少突胶质细胞,抑制O-2A细胞分化成星形胶质细胞。GGF能够促进神经元沿着放射状的胶质细胞迁移,促进培养的视网膜神经元存活和突触生长。 相似文献
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神经病理性疼痛是一种临床的常见疾病,严重影响了患者及家属的生活质量,给社会带来了沉重的负担。神经病理性疼痛的发病机制及有效治疗仍在探索中。中枢神经系统内有三种胶质细胞,包括小胶质细胞、星形胶质细胞以及少突胶质细胞。近来有研究发现,这三种胶质细胞可通过活化、产生和释放细胞因子等途径参与神经病理性疼痛的调节。探索神经胶质细胞的多种复杂功能或作用机制来充分认识胶质细胞的特点,为今后神经病理性疼痛的临床治疗提供新的思路。本文通过研究小胶质细胞、星形胶质细胞以及少突胶质细胞的特点及其对神经病理性疼痛的影响,并分析中枢神经系统胶质细胞与疼痛治疗之间的相关性,旨在总结神经病理性疼痛的发生和发展过程中小胶质细胞、星状胶质细胞及少突胶质细胞的调节作用。 相似文献
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《生理学报》2017,(2)
胶质细胞是脑内数量最多的神经细胞,包括星形胶质细胞、少突胶质前体细胞、NG2胶质细胞等多种类型,具有维持神经系统内环境稳态、支持和营养神经元、调控神经信号传导等多种重要功能。近年来,随着研究的深入,越来越多的证据表明某些特定的胶质细胞在一定条件下表现出干细胞的特性,发挥干细胞的功能。例如,在病理损伤条件下,星形胶质细胞和少突胶质前体细胞均会被活化而出现增殖、分化,体外分离培养可自我更新形成神经球。这些活化的星形胶质细胞和少突胶质前体细胞形成的神经球能够被诱导分化为星形胶质细胞、少突胶质细胞和神经元。此外,通过强制性表达外源基因能将星形胶质细胞和NG2胶质细胞转分化为神经元,这可能也是其干细胞特性的一种体现。本文在已有研究的基础上,总结了放射状胶质细胞、少突胶质前体细胞、星形胶质细胞、NG2胶质细胞与其它类型胶质细胞的干细胞特性、干细胞特性形成的条件、它们可能产生的子代细胞以及涉及的分子信号调控通路。深入探讨胶质细胞的干细胞特性及生理功能,有利于促进其在神经系统损伤修复领域的临床应用。 相似文献
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Huang J Vogel G Yu Z Almazan G Richard S 《The Journal of biological chemistry》2011,286(52):44424-44432
PRMT5 is a type II protein arginine methyltranferase that catalyzes monomethylation and symmetric dimethylation of arginine residues. PRMT5 is functionally involved in a variety of biological processes including embryo development and circadian clock regulation. However, the role of PRMT5 in oligodendrocyte differentiation and central nervous system myelination is unknown. Here we show that PRMT5 expression gradually increases throughout postnatal brain development, coinciding with the period of active myelination. PRMT5 expression was observed in neurons, astrocytes, and oligodendrocytes. siRNA-mediated depletion of PRMT5 in mouse primary oligodendrocyte progenitor cells abrogated oligodendrocyte differentiation. In addition, the PRMT5-depleted oligodendrocyte progenitor and C6 glioma cells expressed high levels of the inhibitors of differentiation/DNA binding, Id2 and Id4, known repressors of glial cell differentiation. We observed that CpG-rich islands within the Id2 and Id4 genes were bound by PRMT5 and were hypomethylated in PRMT5-deficient cells, suggesting that PRMT5 plays a role in gene silencing during glial cell differentiation. Our findings define a role of PRMT5 in glial cell differentiation and link PRMT5 to epigenetic changes during oligodendrocyte differentiation. 相似文献
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He X Takahashi S Suzuki H Hashikawa T Kulkarni AB Mikoshiba K Ohshima T 《Neurochemical research》2011,36(7):1293-1303
Cyclin-dependent kinase 5 (Cdk5) plays a pivotal role in neuronal migration and differentiation, and in axonal elongation.
Although many studies have been conducted to analyze neuronal functions of Cdk5, its kinase activity has also been reported
during oligodendrocyte differentiation, which suggests Cdk5 may play an important role in oligodendrocytes. Here, we describe
a hypomyelination phenotype observed in Emx1-cre mediated Cdk5 conditional knockout (cKO) mice (Emx1-cKO), in which the Cdk5
gene was deleted in neurons, astrocytes and oligodendrocyte -lineage cells. In contrast, the Cdk5 gene in CaMKII cKO mice
was deleted only in neurons. Because the development of mature oligodendrocytes from oligodendrocyte precursor cells is a
complex process, we performed in situ hybridization using markers for the oligodendrocyte precursor cell and for the differentiated
oligodendrocyte. Our results indicate that hypomyelination in Emx1-cKO is due to the impaired differentiation of oligodendrocytes,
rather than to the proliferation or migration of their precursors. The present study confirmed the in vivo role of Cdk5 in
oligodendrocyte differentiation. 相似文献
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Histone modifications affect timing of oligodendrocyte progenitor differentiation in the developing rat brain 总被引:13,自引:0,他引:13 下载免费PDF全文
Timely differentiation of progenitor cells is critical for development. In this study we asked whether global epigenetic mechanisms regulate timing of progenitor cell differentiation into myelin-forming oligodendrocytes in vivo. Histone deacetylation was essential during a specific temporal window of development and was dependent on the enzymatic activity of histone deacetylases, whose expression was detected in the developing corpus callosum. During the first 10 postnatal days, administration of valproic acid (VPA), the specific inhibitor for histone deacetylase activity, resulted in significant hypomyelination with delayed expression of late differentiation markers and retained expression of progenitor markers. Differentiation resumed in VPA-injected rats if a recovery period was allowed. Administration of VPA after myelination onset had no effect on myelin gene expression and was consistent with changes of nucleosomal histones from reversible deacetylation to more stable methylation and chromatin compaction. Together, these data identify global modifications of nucleosomal histones critical for timing of oligodendrocyte differentiation and myelination in the developing corpus callosum. 相似文献
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