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The Journal of Neuroscience, April 15, 1999, 19(8):3043-3049

Oligodendrocyte Apoptosis Mediated by Caspase Activation

Chenghua Gu², Patrizia Casaccia-Bonnefil¹, Anu Srinivasan³, and Moses V. Chao¹

¹ Molecular Neurobiology Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, ² Cell Biology Program, Weill Graduate School of Cornell University Medical College, New York, New York 10021, and ³ IDUN Pharmaceuticals Inc., La Jolla, California 92037

Treatment with NGF causes long-term cultures of oligodendrocytes to die via a yet undefined mechanism mediated by the p75 neurotrophin receptor. The p75 receptor belongs to the TNF receptor superfamily of molecules, which includes Fas and p55 TNF receptors. The Fas and TNF receptors use adaptor molecules to recruit and activate caspase-8 to the receptor. Using a combination of immunohistochemical and Western blotting assays, we have examined caspase activity during NGF-induced apoptosis. Interestingly, although caspase-1 [interleukin-1-converting enzyme (ICE)], caspase-2, caspase-3, and caspase-8 were expressed in oligodendrocytes, only caspase-1, -2, and -3 were activated after NGF treatment, whereas caspase-8 was not. These data suggest that the mechanism of apoptosis by NGF through the p75 receptor is different from TNF and Fas-mediated killing.  Radiation of oligodendrocytes also activated a similar subset of caspases as NGF, indicating that NGF-induced oligodendrocyte apoptosis uses a similar cell death execution mechanism as injury models. This consolidates a potential role of the p75 neurotrophin receptor during stress and inflammatory conditions.

Key words: apoptosis; p75 neurotrophin receptor; NGF; caspase; TNF; Fas; oligodendrocyte

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Copyright © 1999 Society for Neuroscience  0270-6474/99/1983043-07$05.00/0

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