Polydendrocytes: NG2 Cells with Many Roles in Development and Repair of the CNS

Nishiyama, Akiko

doi:10.1177/1073858406295586

Cited by 151 publications

(128 citation statements)

References 121 publications

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“…Oligodendrocytes provide myelin sheaths for enhanced axonal transmission (Wood and Bunge, 1984) but they or their progenitors can also remyelinate under certain circumstances (Chang et al, 2000;Nishiyama, 2007;Trotter, 2005;Wilson et al, 2006). Microglial cells are the resident immune system phagocytic cells within the brain and spinal cord (Kim and de Vellis, 2005), and they also respond rapidly for neural protection or healing after injury (Davalos et al, 2005;Wu et al, 2007b).…”

Section: Introductionmentioning

confidence: 99%

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Fitch

Silver

2008

Experimental Neurology

867

657

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Spinal cord and brain injuries lead to complex cellular and molecular interactions within the central nervous system in an attempt to repair the initial tissue damage. Many studies have illustrated the importance of the glial cell response to injury, and the influences of inflammation and wound healing processes on the overall morbidity and permanent disability that result. The abortive attempts of neuronal regeneration after spinal cord injury are influenced by inflammatory cell activation, reactive astrogliosis and the production of both growth promoting and inhibitory extracellular molecules. Despite the historical perspective that the glial scar was a mechanical barrier to regeneration, inhibitory molecules in the forming scar and methods to overcome them have suggested molecular modification strategies to allow neuronal growth and functional regeneration. Unlike myelin associated inhibitory molecules, which remain at largely static levels before and after central nervous system trauma, inhibitory extracellular matrix molecules are dramatically upregulated during the inflammatory stages after injury providing a window of opportunity for the delivery of candidate therapeutic interventions. While high dose methylprednisolone steroid therapy alone has not proved to be the solution to this difficult clinical problem, other strategies for modulating inflammation and changing the make up of inhibitory molecules in the extracellular matrix are providing robust evidence that rehabilitation after spinal cord and brain injury has the potential to significantly change the outcome for what was once thought to be permanent disability.

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Section: Introductionmentioning

confidence: 99%

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Fitch

Silver

2008

Experimental Neurology

867

657

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“…It is therefore well conceivable that the Olig2-derived cells are arrested in an "immature," although postmitotic state. These NG2 ϩ glial cells could then perform specific physiological functions (Butt et al, 2002;Greenwood and Butt, 2003;Paukert and Bergles, 2006;Nishiyama, 2007;Káradó ttir et al, 2008), although it is not clear whether NG2…”

Section: Mechanisms Mediating Distinct Progeny Of Olig2mentioning

confidence: 99%

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Dimou¹,

Simon²,

Kirchhoff³

et al. 2008

J. Neurosci.

478

564

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Despite their abundance, still little is known about the rather frequent, constantly proliferating progenitors spread throughout the adult mouse brain parenchyma. The majority of these progenitors express the basic-helix-loop-helix transcription factor Olig2, and their number further increases after injury. Here, we examine the progeny of this progenitor population by genetic fate mapping using tamoxifen-inducible Cre-recombination in the Olig2 locus to turn on permanent reporter gene expression in the adult brain. Consistent with Olig2 expression in proliferating NG2 ϩ progenitors, most reporter ϩ cells seen shortly after initiating recombination at adult stages incorporated BrdU and contained the proteoglycan NG2 in both the gray (GM) and the white matter (WM) of the cerebral cortex. However, at longer time points after induction, we observed profound differences in the identity of reporter ϩ cells in the WM and GM. Whereas most of the Olig2 ϩ progenitors had generated mature, myelinating oligodendrocytes in the WM, hardly any reporter ϩ cells showing mature oligodendrocyte characteristics were detectable even up to 6 months after recombination in the GM. In the GM, most reporter ϩ cells remained NG2 ϩ , even after injury, but stopped proliferating rather soon after recombination. Thus, our results demonstrate the continuous generation of mature, myelinating oligodendrocytes in the WM, whereas cells in the GM generated mostly postmitotic NG2 ϩ glia.

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“…They represent a cell population in the developing and mature central nervous system (CNS) that is distinct from neurons, astrocytes, mature oligodendrocytes and resting microglia (Nishiyama, 2007;Nishiyama et al, 2009). They generate oligodendrocytes in vitro (Levine and Stallcup, 1987;Stallcup and Beasley, 1987) and in vivo (Zhu et al, 2008a;Zhu et al, 2008b;Rivers et al, 2008;Dimou et al, 2008;Zhu et al, 2011), and are hence also referred to as oligodendrocyte precursor cells (OPCs).…”

Section: Introductionmentioning

confidence: 99%

Olig2-dependent developmental fate switch of NG2 cells

et al. 2012

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SUMMARYNG2-expressing cells (NG2 cells or polydendrocytes) generate oligodendrocytes throughout the CNS and a subpopulation of protoplasmic astrocytes in the gray matter of the ventral forebrain. The mechanisms that regulate their oligodendrocyte or astrocyte fate and the degree to which they exhibit lineage plasticity in vivo have remained unclear. The basic helix-loop-helix transcription factor Olig2 is required for oligodendrocyte specification and differentiation. We have found that Olig2 expression is spontaneously downregulated in NG2 cells in the normal embryonic ventral forebrain as they differentiate into astrocytes. To further examine the role of Olig2 in NG2 cell fate determination, we used genetic fate mapping of NG2 cells in constitutive and tamoxifen-inducible Olig2 conditional knockout mice in which Olig2 was deleted specifically in NG2 cells. Constitutive deletion of Olig2 in NG2 cells in the neocortex and corpus callosum but not in ventral forebrain caused them to convert their fate into astrocytes, with a concomitant severe reduction in the number of oligodendrocytes and myelin. Deletion of Olig2 in NG2 cells in perinatal mice also resulted in astrocyte generation from neocortical NG2 cells. These observations indicate that the developmental fate of NG2 cells can be switched by altering a single transcription factor Olig2.

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Polydendrocytes: NG2 Cells with Many Roles in Development and Repair of the CNS

Cited by 151 publications

References 121 publications

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Olig2-dependent developmental fate switch of NG2 cells

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