Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 35, Issue 1, Pages 171-182Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2007.02.012
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- NINDS NIH HHS [R01 NS39159, R01 NS043422-01, R01 NS043422-03, R01 NS043422, R01 NS039159, R01 NS43422, R01 NS043422-02] Funding Source: Medline
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Bone morphogenetic proteins have been implicated in the development of oligodendrocytes and astrocytes, however, a role for endogenous BMP signaling in glial development has not been demonstrated in a genetic model. Using mice in which signaling via type I BMP receptors Bmpr1a and Bmpr1b have been inactivated in the neural tube, we demonstrate that BMP signaling contributes to the maturation of glial cells in vivo. At PO, mutant mice exhibited a 25-40% decrease in GFAP + or S100 beta+ astrocytes in the cervical spinal cord. The number of oligodendrocyte precursors and the timing of their emergence was unchanged in the mutant mice compared to the normals, however myelin protein expression and mature oligodendrocyte numbers were significantly reduced. These data indicate that BMP signaling promotes the generation of astrocytes and mature, myelinating oligodendrocytes in vivo but does not affect oligodendrocyte precursor development, thus suggesting tight regulation of BMP signaling to ensure proper gliogenesis. (C) 2007 Elsevier Inc. All rights reserved.
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