期刊
NEUROBIOLOGY OF DISEASE
卷 15, 期 1, 页码 120-131出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2003.09.002
关键词
autoantibody; glia; multiple sclerosis; apoptosis; myelin; demyelinating disease
资金
- NICHD NIH HHS [HD07447-10R] Funding Source: Medline
- NINDS NIH HHS [NS40209, NS32129, NS24180] Funding Source: Medline
Stabilizing the survival of oligodendrocytes and oligodendrocyte precursors within and near lesions in patients suffering from multiple sclerosis (MS) and other demyelinating diseases is an important therapeutic goal. Previous studies have identified a human-derived monoclonal IgM antibody designated rHIgM22 that induces remyelination in a mouse model of MS. We provide evidence that this antibody, directed against myelin, induces antiapoptotic signaling in premyelinating oligodendrocytes and reduces caspase-3 activation and caspase gene expression in mice undergoing antibody-induced remyelination. This effect was dependent on calcium entry via CNQX-sensitive channels and on lipid raft integrity, and was correlated with suppression of JNK signaling. We conclude that rHIgM22 may induce remyelination via rescue of oligodendrocytes, and suggest that such autoantibody-mediated signaling may have important therapeutic implications for a variety of neurological diseases, including stroke and Alzheimer's disease. (C) 2003 Elsevier Inc. All rights reserved.
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