Endogenous Brain Repair: Overriding intrinsic lineage determinates through injury-induced micro-environmental signals.

Neurogenesis (Austin, Tex.) Pub Date : 2017-05-23 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1297881
Kathryn S Jones, Bronwen Connor
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引用次数: 2

Abstract

Adult human neurogenesis has generated excitement over the last 2 decades with the idea that endogenous adult stem cells could act as a potential cell source for brain repair after injury. Indeed, many forms of experimentally induced brain injury including stroke and excitotoxic lesioning can promote proliferation from the subventricular zone and mobilise neuroblasts and oligodendrocyte progenitor cells to migrate through brain parenchyma to damaged regions. However the failure of neuroblasts to mature into appropriate neuronal subtypes for cell replacement has been an issue. Recent work by our group and others has indicated that micro-environmental signals released from areas of cell loss may be able to override intrinsic gene expression lineages and covert neuroblasts into oligodendrocyte progenitor cells. This commentary will discuss the enhanced fate plasticity of both adult neural progenitors and parenchymal NG2 cells after injury, and the importance of understanding brain-injury induced micro-environmental signals in the quest toward promoting endogenous regeneration after injury.

内源性脑修复:通过损伤诱导的微环境信号决定的超越内在谱系。
在过去的20年里,由于内源性成体干细胞可以作为脑损伤后修复的潜在细胞来源,成人神经发生已经引起了人们的兴奋。事实上,许多形式的实验性脑损伤,包括中风和兴奋性毒性损伤,都可以促进脑室下区增殖,并动员神经母细胞和少突胶质细胞祖细胞通过脑实质迁移到受损区域。然而,神经母细胞未能成熟为适合细胞替代的神经元亚型一直是一个问题。我们小组和其他人最近的工作表明,从细胞丢失区域释放的微环境信号可能能够覆盖内在的基因表达谱系,并将神经母细胞转化为少突胶质细胞祖细胞。本文将讨论损伤后成人神经祖细胞和实质NG2细胞命运可塑性的增强,以及理解脑损伤诱导的微环境信号对促进损伤后内源性再生的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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