| First Author | Arnett HA | Year | 2001 |
| Journal | Nat Neurosci | Volume | 4 |
| Issue | 11 | Pages | 1116-22 |
| PubMed ID | 11600888 | Mgi Jnum | J:72695 |
| Mgi Id | MGI:2153408 | Doi | 10.1038/nn738 |
| Citation | Arnett HA, et al. (2001) TNFalpha promotes proliferation of oligodendrocyte progenitors and remyelination. Nat Neurosci 4(11):1116-22 |
| abstractText | Here we used mice lacking tumor necrosis factor-alpha (TNFalpha) 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 TNFalpha 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 TNFalpha in the CNS is important for understanding oligodendrocyte regeneration/proliferation, nerve remyelination and the design of new therapeutics for demyelinating diseases. |
