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出生后啮齿动物大脑中少突胶质细胞亚群中塌陷反应介导蛋白(CRMP/ULIP)的差异表达。

Differential expression of collapsin response mediator proteins (CRMP/ULIP) in subsets of oligodendrocytes in the postnatal rodent brain.

作者信息

Ricard D, Stankoff B, Bagnard D, Aguera M, Rogemond V, Antoine J C, Spassky N, Zalc B, Lubetzki C, Belin M F, Honnorat J

机构信息

INSERM U433 Hôpital Neurologique, Lyon, France.

出版信息

Mol Cell Neurosci. 2000 Oct;16(4):324-37. doi: 10.1006/mcne.2000.0888.

DOI:10.1006/mcne.2000.0888
PMID:11085871
Abstract

The family of collapsin response mediator protein/Unc-33-like protein (CRMP/Ulip), composed of four homologous members, is specifically and highly expressed in the nervous system during embryonic neuronal development and dramatically down-regulated in the adult. Members of this family have been proposed to be part of the semaphorins signal transduction pathway involved in axonal outgrowth. Here, we show by in situ hybridization and immunohistochemistry that CRMP2/Ulip2, and to a lesser extent CRMP3/Ulip4, are expressed in immature and mature oligodendrocytes, but not in astrocytes. Transcripts encoding the other CRMP/Ulip members are also detectable by RT-PCR in highly purified mature oligodendrocytes. Interestingly, in the adult, the protein CRMP2/Ulip2 is mainly detectable in subsets of oligodendrocytes distributed according to an increasing rostrocaudal gradient, with the largest number of positive cells being present in the brain stem and spinal cord. In cultures of highly purified oligodendrocytes, however, CRMP2/Ulip2 was detectable in all the cells. Addition of Sema3A in the culture medium completely inhibited the emergence of oligodendrocyte processes suggesting that, as in neurons, a Sema3A signaling pathway mediated via CRMP2/Ulip2 may be involved in the regulation of oligodendroglial process outgrowth.

摘要

塌陷反应介导蛋白/Unc-33样蛋白(CRMP/Ulip)家族由四个同源成员组成,在胚胎神经元发育过程中于神经系统中特异性高表达,而在成体中显著下调。该家族成员被认为是参与轴突生长的信号素信号转导途径的一部分。在此,我们通过原位杂交和免疫组织化学表明,CRMP2/Ulip2以及程度较轻的CRMP3/Ulip4在未成熟和成熟少突胶质细胞中表达,但在星形胶质细胞中不表达。通过RT-PCR在高度纯化的成熟少突胶质细胞中也可检测到编码其他CRMP/Ulip成员的转录本。有趣的是,在成体中,蛋白CRMP2/Ulip2主要在根据尾头梯度递增分布的少突胶质细胞亚群中可检测到,脑干和脊髓中阳性细胞数量最多。然而,在高度纯化的少突胶质细胞培养物中,所有细胞均可检测到CRMP2/Ulip2。在培养基中添加信号素3A完全抑制了少突胶质细胞突起的出现,这表明正如在神经元中一样,经由CRMP2/Ulip2介导的信号素3A信号通路可能参与少突胶质细胞突起生长的调控。

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