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The Journal of Neuroscience, February 15, 1998, 18(4):1297-1304
p75 Neurotrophin Receptor Expression on Adult Human
Oligodendrocytes: Signaling without Cell Death in Response to
NGF
Uma
Ladiwala1,
Christian
Lachance2,
Steve
J. J.
Simoneau2,
Asha
Bhakar2,
Philip A.
Barker2 and
Jack P.
Antel1
1 Neuroimmunology Unit and 2 Center for
Neuronal Survival, Montreal Neurological Institute, McGill University,
Montreal, Quebec H3A 2B4, Canada
Oligodendrocytes (OLs) are the primary targets in the autoimmune
disease multiple sclerosis (MS). Cell receptors belonging to the tumor
necrosis factor receptor (TNF-R) superfamily, such as TNF receptors and
fas, are implicated in signaling the injury response of OLs. The p75
neurotrophin receptor (p75NTR), another member of
the TNF-R superfamily, has been reported to mediate nerve growth factor
(NGF)-induced apoptosis in some neural systems. To address the
potential relationship between p75NTR signaling and
OL injury, we assayed adult human OLs cultured under several different
conditions for p75NTR and tyrosine kinase receptor
trkA expression, for NGF-mediated apoptosis, and for NGF-mediated jun
kinase (JNK) or nuclear factor (NF)  B activation. In the current
study, we have found expression of p75NTR on
cultured adult CNS-derived human OLs but not on other glial cells. TrkA
was not detected on these OLs in any of the culture conditions tested.
Treatment of the OLs with varying concentrations of NGF over a range of
time periods resulted in no significant increase in numbers of terminal
transferase (TdT)-mediated d-uridine triphosphate (UTP)-biotin nick-end
labeling positive OLs, whereas significant cell death was observed
using TNF- . Furthermore, unlike TNF- treatment, NGF treatment did
not significantly activate JNK, although both TNF- and NGF induced
nuclear translocation of NF-B. These findings contrast with the
recent report of NGF-mediated apoptosis in the OLs of neonatal rats
matured in vitro, which express
p75NTR but not trkA (), and suggest that, at least in humans, p75NTR
signaling may mediate responses other than apoptosis of OLs.
Key words:
p75NTR; oligodendrocytes; human; trkA; NGF; apoptosis; multiple sclerosis; JNK; NF-B
Copyright © 1998 Society for Neuroscience 0270-6474/98/1841297-08$05.00/0
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