Oligodendrocyte maturation is inhibited by bone morphogenetic protein

See, Jill; Zhang, Xianchao; Eraydin, Nuri; Mun, Sung-Bin; Mamontov, Polina; Golden, Jeffrey A.; Grinspan, Judith B.

doi:10.1016/j.mcn.2004.04.004

Cited by 115 publications

(126 citation statements)

References 35 publications

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“…Overexpression studies of BMPs include the addition of BMPs to in vitro culture systems which inhibits differentiation of OPCs and myelin protein expression but promotes astrocyte development (Grinspan et al, 2000;Gross et al, 1996;Mabie et al, 1997;See et al, 2004). In vivo experiments in which BMPs are overexpressed from neuron-specific promoters, or are over-expressed locally via bead implantation in Xenopus or implantation of BMPoverexpressing cells in chick indicate that BMPs promote astrogliogenesis while inhibiting oligodendrocyte development (Gomes et al, 2003;Mekki-Dauriac et al, 2002;Miller et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…(Pierce Chemical, Rockford, IL). Protein samples (50μg) were denatured and run on 15% gel as previously described (See et al, 2004). Membranes were incubated in blocking buffer with anti-MBP (1:500) and anti-GFAP (1:100).…”

Section: Western Blottingmentioning

confidence: 99%

“…Antibodies used for immunolabeling cultures cells were anti-phospho-Smad (Cell Signaling), A2B5 (hybridoma supernatant, ATCC, (Eisenbarth et al, 1979), 01 and PLP. Procedures for immunolabeling oligodendrocytes in culture have been described previously (See et al, 2004).…”

Section: Cell Culturementioning

confidence: 99%

“…BMPs have also been hypothesized to regulate the development of both oligodendrocytes and astrocytes. In vitro, addition of BMPs to culture systems promotes astrogliogenesis and inhibits oligodendrogliogenesis (Grinspan et al, 2000;Mabie et al, 1997;See et al, 2004). In vivo, application of BMPs in developing spinal cord decreases the number of differentiated oligodendrocytes (Mekki-Dauriac et al, 2002;Miller et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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BMP signaling mutant mice exhibit glial cell maturation defects

See

Mamontov

Ahn

et al. 2007

Molecular and Cellular Neuroscience

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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 P0, mutant mice exhibited a 25-40% decrease in GFAP+ or S100β+ 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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Section: Discussionmentioning

confidence: 99%

Section: Western Blottingmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

BMP signaling mutant mice exhibit glial cell maturation defects

See

Mamontov

Ahn

et al. 2007

Molecular and Cellular Neuroscience

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“…Primary hippocampal and cortical cultures were prepared from embryonic rat pups as described previously (Wilcox and Dichter, 1994) and plated on poly-L-lysine-coated plates with Neurobasal medium (Invitrogen).Cultures were allowed to grow for 5 d before harvesting for reverse transcription (RT)-PCR (see below). Purified rat oligodendrocyte cultures were prepared as described by See et al (2004). Final purification of the cultures was done by immunopanning, which created a 94% pure oligodendrocyte culture (the remaining 6% were GFAP-positive astrocytes).…”

Section: Methodsmentioning

confidence: 99%

MONaKA, a Novel Modulator of the Plasma Membrane Na,K-ATPase

Mao¹,

Ferguson²,

Cibulsky³

et al. 2005

J. Neurosci.

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We have cloned and characterized mouse and human variants of MONaKA, a novel protein that interacts with and modulates the plasma membrane Na,K-ATPase. MONaKA was cloned based on its sequence homology to the Drosophila Slowpoke channel-binding protein dSlob, but mouse and human MONaKA do not bind to mammalian Slowpoke channels. At least two splice variants of MONaKA exist; the splicing is conserved perfectly between mouse and human, suggesting that it serves some important function. Both splice variants of MONaKA are expressed widely throughout the CNS and peripheral nervous system, with different splice variant expression ratios in neurons and glia. A yeast two-hybrid screen with MONaKA as bait revealed that it binds tightly to the ␤1 and ␤3 subunits of the Na,K-ATPase. The association between MONaKA and Na,K-ATPase ␤ subunits was confirmed further by coimmunoprecipitation from transfected cells, mouse brain, and cultured mouse astrocytes. A glutathione S-transferase-MONaKA fusion protein inhibits Na,KATPase activity from whole brain or cultured astrocytes. Furthermore, transfection of MONaKA inhibits 86 Rb ϩ uptake via the Na,KATPase in intact cells. These results are consistent with the hypothesis that MONaKA modulates brain Na,K-ATPase and may thereby participate in the regulation of electrical excitability and synaptic transmission.

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The complex world of oligodendroglial differentiation inhibitors

Kremer

Aktaş

Hartung

et al. 2011

Annals of Neurology

121

101

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Myelination is a central nervous system (CNS) process wherein oligodendrocyte-axon interactions lead to the establishment of myelin sheaths that stabilize, protect, and electrically insulate axons. In inflammatory demyelinating diseases such as multiple sclerosis (MS), the degeneration and eventual loss of functional myelin sheaths slows and blocks saltatory conduction in axons, which results in clinical impairment. However, remyelination can occur, and lesions can be partially repaired, resulting in clinical remission. The recruitment and activation of resident oligodendrocyte precursor cells (OPCs) play a critical role in the repair process because these cells have the capacity to differentiate into functional myelinating cells. Mature oligodendrocytes, however, are thought to have lost the capacity to develop new myelin sheaths and frequently undergo programmed cell death in MS. The endogenous capacity to generate new oligodendrocytes in MS is limited, and this is predominantly due to the presence of inhibitory components that block OPC differentiation and maturation. Here, we present an overview of recently identified negative regulators of oligodendroglial differentiation and their potential relevance for CNS repair in MS. Because currently available immunomodulatory drugs for MS mainly target inflammatory cascades outside the brain and fail to repair existing lesions, achieving more efficient lesion repair constitutes an important goal for future MS therapies.

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Oligodendrocyte maturation is inhibited by bone morphogenetic protein

Cited by 115 publications

References 35 publications

BMP signaling mutant mice exhibit glial cell maturation defects

BMP signaling mutant mice exhibit glial cell maturation defects

MONaKA, a Novel Modulator of the Plasma Membrane Na,K-ATPase

The complex world of oligodendroglial differentiation inhibitors

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