PMID- 11600888
OWN - NLM
STAT- MEDLINE
DCOM- 20011207
LR  - 20220321
IS  - 1097-6256 (Print)
IS  - 1097-6256 (Linking)
VI  - 4
IP  - 11
DP  - 2001 Nov
TI  - TNF alpha promotes proliferation of oligodendrocyte progenitors and 
      remyelination.
PG  - 1116-22
AB  - Here we used mice lacking tumor necrosis factor-alpha (TNF alpha) and its 
      associated receptors to study a model of demyelination and remyelination in which 
      these events could be carefully controlled using a toxin, cuprizone. 
      Unexpectedly, the lack of TNF alpha led to a significant delay in remyelination 
      as assessed by histology, immunohistochemistry for myelin proteins and electron 
      microscopy coupled with morphometric analysis. Failure of repair correlated with 
      a reduction in the pool of proliferating oligodendrocyte progenitors 
      (bromodeoxyuridine-labeled NG2(+) cells) followed by a reduction in the number of 
      mature oligodendrocytes. Analysis of mice lacking TNF receptor 1 (TNFR1) or TNFR2 
      indicated that TNFR2, not TNFR1, is critical to oligodendrocyte regeneration. 
      This unexpected reparative role for TNF alpha in the CNS is important for 
      understanding oligodendrocyte regeneration/proliferation, nerve remyelination and 
      the design of new therapeutics for demyelinating diseases.
FAU - Arnett, H A
AU  - Arnett HA
AD  - Lineberger Comprehensive Cancer Center, School of Medicine CB7295, University of 
      North Carolina, Chapel Hill, North Carolina 27599, USA.
FAU - Mason, J
AU  - Mason J
FAU - Marino, M
AU  - Marino M
FAU - Suzuki, K
AU  - Suzuki K
FAU - Matsushima, G K
AU  - Matsushima GK
FAU - Ting, J P
AU  - Ting JP
LA  - eng
GR  - NS34190/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Nat Neurosci
JT  - Nature neuroscience
JID - 9809671
RN  - 0 (Antigens, CD)
RN  - 0 (Monoamine Oxidase Inhibitors)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 5N16U7E0AO (Cuprizone)
SB  - IM
MH  - Animals
MH  - Antigens, CD/genetics/*metabolism
MH  - Apoptosis
MH  - B-Lymphocytes/metabolism
MH  - Brain Chemistry
MH  - Corpus Callosum/metabolism/ultrastructure
MH  - Cuprizone/administration & dosage/toxicity
MH  - Demyelinating Diseases/chemically induced
MH  - Disease Models, Animal
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Macrophages/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Microglia/metabolism
MH  - Monoamine Oxidase Inhibitors/pharmacology
MH  - Myelin Sheath/*metabolism/pathology/ultrastructure
MH  - Oligodendroglia/cytology/drug effects/*physiology
MH  - Receptors, Tumor Necrosis Factor/genetics/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Stem Cells/*physiology/ultrastructure
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism
MH  - Up-Regulation
EDAT- 2001/10/16 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/10/16 10:00
PHST- 2001/10/16 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/16 10:00 [entrez]
AID - nn738 [pii]
AID - 10.1038/nn738 [doi]
PST - ppublish
SO  - Nat Neurosci. 2001 Nov;4(11):1116-22. doi: 10.1038/nn738.