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J. Biol. Chem., Vol. 281, Issue 29, 99922, July 21, 2006
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Interfer-ing with Myelin{diamondsuit}

Inflammatory reactions in the central nervous system play important roles in the pathogenesis of white matter diseases such as multiple sclerosis and periventricular leukomalacia. These reactions result in the exposure of oligodendrocytes to various cytokines that affect oligodendroglial survival, proliferation, and differentiation. One of these cytokines, interferon-{gamma} (IFNG), has been reported to have both a deleterious and protective role on myelin synthesis. These conflicting observations prompted Makoto Horiuchi and colleagues to investigate the effects of interferon-{gamma} on rat oligodendroglial cultures at different developmental stages.Go


Figure 1
IFNG induces cell death in oligodendroglial progenitor cells.

In this Paper of the Week, the researchers show that simultaneous activation of the signal transducers and activator of transcription (STAT) pathway by interferon-{gamma} and of the extracellular signal-regulated kinase (ERK) pathway by exogenous trophic factors plays a role in interferon-induced cytotoxicity in proliferating oligodendroglial progenitors. The effect is developmental stage-specific in that non-proliferating immature and mature oligodendrocytes are protected from interferon-induced cell death. This comprehensive study is of considerable importance and relevance to inflammation-induced demyelinating disease.

FOOTNOTES

{diamondsuit} See referenced article, J. Biol. Chem. 2006, 281, 20095-20106 Back



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This Article
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Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.
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