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蝾螈脑的祖细胞在稳态和神经元再生期间的动力学。

Progenitor cell dynamics in the Newt Telencephalon during homeostasis and neuronal regeneration.

机构信息

Department of Cell and Molecular Biology, Karolinska Institutet, Berzelius väg 35, 171 77 Stockholm, Sweden.

出版信息

Stem Cell Reports. 2014 Mar 20;2(4):507-19. doi: 10.1016/j.stemcr.2014.01.018. eCollection 2014 Apr 8.

DOI:10.1016/j.stemcr.2014.01.018
PMID:24749074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3986684/
Abstract

The adult newt brain has a marked neurogenic potential and is highly regenerative. Ventricular, radial glia-like ependymoglia cells give rise to neurons both during normal homeostasis and after injury, but subpopulations among ependymoglia cells have not been defined. We show here that a substantial portion of GFAP(+) ependymoglia cells in the proliferative hot spots of the telencephalon has transit-amplifying characteristics. In contrast, proliferating ependymoglia cells, which are scattered along the ventricular wall, have stem cell features in terms of label retention and insensitivity to AraC treatment. Ablation of neurons remodels the proliferation dynamics and leads to de novo formation of regions displaying features of neurogenic niches, such as the appearance of cells with transit-amplifying features and proliferating neuroblasts. The results have implication both for our understanding of the evolutionary diversification of radial glia cells as well as the processes regulating neurogenesis and regeneration in the adult vertebrate brain.

摘要

成体蝾螈脑具有显著的神经发生潜力和高度的再生能力。室管膜下胶质细胞(ependymoglia cells)在正常的稳态和损伤后都能产生神经元,但ependymoglia 细胞的亚群尚未确定。我们在这里表明,在端脑的增殖热点中,相当一部分 GFAP(+)ependymoglia 细胞具有过渡扩增特征。相比之下,沿脑室壁分布的增殖ependymoglia 细胞具有干细胞特征,表现为标记保留和对 AraC 处理不敏感。神经元的缺失会重塑增殖动力学,并导致新的具有神经发生龛特征的区域形成,例如出现具有过渡扩增特征和增殖性神经母细胞的细胞。这些结果不仅对我们理解径向胶质细胞的进化多样化有影响,而且对调节成年脊椎动物大脑中的神经发生和再生的过程也有影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/24dbb49c3986/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/26b687696af7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/a84d20406da9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/e698ac8febe3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/3ce8f73c8b0f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/83e5b6bca892/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/f1486b31148d/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/24dbb49c3986/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/26b687696af7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/a84d20406da9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/e698ac8febe3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/3ce8f73c8b0f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/83e5b6bca892/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/f1486b31148d/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42c9/3986684/24dbb49c3986/gr7.jpg

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