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Expression of the low‐affinity neurotrophin receptor, p75 NTR , is upregulated by oligodendroglial progenitors adjacent to the subventricular zone in response to demyelination
Precursor cells have the capacity to repopulate the demyelinated brain, but the molecular mechanisms that facilitate their recruitment are largely unknown. The low‐affinity neurotrophin receptor, p75 NTR , may be one of these regulators; however, its expression profile by oligodendroglia within the...
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Published in: | Glia 2004-10, Vol.48 (1), p.64-75 |
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Main Authors: | , , , , , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Precursor cells have the capacity to repopulate the demyelinated brain, but the molecular mechanisms that facilitate their recruitment are largely unknown. The low‐affinity neurotrophin receptor, p75
NTR
, may be one of these regulators; however, its expression profile by oligodendroglia within the multiple sclerosis (MS) brain remains uncertain. We therefore assessed the expression profile of this receptor within 8 MS and 4 control brains. We found no evidence of expression of p75
NTR
by mature oligodendrocytes. Instead, we demonstrated the presence of p75
NTR
on a subgroup of NG2‐positive oligodendroglial progenitors in a periventricular plaque in one MS sample. Notably, p75
NTR
‐expressing cells were also detected within the subventricular zone (SVZ) of this brain, adjacent to the periventricular plaque. In animals with experimental demyelination we observed similar patterns of p75
NTR
expression, initially confined to precursor cells within the SVZ, followed at later stages in the disease course by its expression amongst a subset of oligodendroglial progenitors within the corpus callosum. These data suggest that a population of precursor cells within the SVZ can be induced to express p75
NTR
and to subsequently assume an oligodendroglial progenitor phenotype in response to demyelination in the adjacent white matter. © 2004 Wiley‐Liss, Inc. |
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ISSN: | 0894-1491 1098-1136 |
DOI: | 10.1002/glia.20056 |