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Publication : BMP signaling mutant mice exhibit glial cell maturation defects.

First Author  See J Year  2007
Journal  Mol Cell Neurosci Volume  35
Issue  1 Pages  171-82
PubMed ID  17391983 Mgi Jnum  J:123227
Mgi Id  MGI:3717526 Doi  10.1016/j.mcn.2007.02.012
Citation  See J, et al. (2007) BMP signaling mutant mice exhibit glial cell maturation defects. Mol Cell Neurosci 35(1):171-82
abstractText  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 P0, mutant mice exhibited a 25-40% decrease in GFAP+ or S100beta+ 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.
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