Common Developmental Requirement for Olig Function Indicates a Motor Neuron/Oligodendrocyte Connection

Lü, Qing; Sun, Tao; Zhu, Zhimin; Ma, Nan; García, Meritxell Aguiló; Stiles, Charles D.; Rowitch, David H.

doi:10.1016/s0092-8674(02)00678-5

Cited by 962 publications

(1,061 citation statements)

References 40 publications

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“…If the oligodendrocyte precursors were unable to mature or were delayed in maturation, the O4 number would stay the same. Finally, these data mirror those found in mice with genetically eliminated expression of Olig1, Nkx2.2, Sox 10, transcription factors required for oligodendrocyte development (Lu et al, 2002;Qi et al, 2001;Stolt et al, 2002). These knockout models showed normal numbers of OPCs and delayed or decreased oligodendrocyte differentiation without adoption of another cell fate.…”

Section: Discussionsupporting

confidence: 72%

“…Oligodendrocytes initially appear as oligodendrocyte precursor cells (OPCs) that first originate from the ventral ventricular zone which lies dorsal to the floor plate (Ono et al, 1995;Pringle and Richardson, 1993). The expression of sonic hedgehog specifies the ventral location and induces the expression of transcription factors, such as Olig1 and 2, necessary for oligodendrocyte specification and development (Lu et al, 2002;Lu et al, 2000;Zhou and Anderson, 2002;Zhou et al, 2000). Inhibitors of oligodendrocyte development in the roof plate have been hypothesized to repress OPC formation in the dorsal neural tube (Wada et al, 2000).…”

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: Discussionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

BMP signaling mutant mice exhibit glial cell maturation defects

See

Mamontov

Ahn

et al. 2007

Molecular and Cellular Neuroscience

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“…Olig2 is a basic helix-loop-helix (bHLH) transcription factor that is uniquely expressed in neural stem cells or progenitors in the central nervous system (CNS). Olig2 is highly expressed in neural progenitors that give rise to oligodendrocytes and several subtypes of neurons (Lu et al, 2002). A number of studies have shown that Olig2 is widely expressed in astrocytomas and is required for tumor initiation and growth in vivo (Ligon et al, 2004;, suggesting a functional link between Olig2 expression and cancer stem cells in gliomas.…”

Section: Specific Transcription Factors and The Maintenance Of Glioblmentioning

confidence: 99%

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

et al. 2010

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Glioblastomas (GBMs) are highly lethal primary brain tumors. Despite current therapeutic advances in other solid cancers, the treatment of these malignant gliomas remains essentially palliative. GBMs are extremely resistant to conventional radiation and chemotherapies. We and others have demonstrated that a highly tumorigenic subpopulation of cancer cells called GBM stem cells (GSCs) promotes therapeutic resistance. We also found that GSCs stimulate tumor angiogenesis by expressing elevated levels of VEGF and contribute to tumor growth, which has been translated into a useful therapeutic strategy in the treatment of recurrent or progressive GBMs. Furthermore, stem cell-like cancer cells (cancer stem cells) have been shown to promote metastasis. Although GBMs rarely metastasize beyond the central nervous system, these highly infiltrative cancers often invade into normal brain tissues preventing surgical resection, and GSCs display an aggressive invasive phenotype. These studies suggest that targeting GSCs may effectively reduce tumor recurrence and significantly improve GBM treatment. Recent studies indicate that cancer stem cells share core signaling pathways with normal somatic or embryonic stem cells, but also display critical distinctions that provide important clues into useful therapeutic targets. In this review, we summarize the current understanding and advances in glioma stem cell research, and discuss potential targeting strategies for future development of anti-GSC therapies.

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“…one important transcription factor is Olig2. The initial specification of the oligodendrocyte lineage is dependent on olig2 and this lineage is absent from olig2-null mice [17] . olig2 induces transcription factors that are required for the generation of mature, postmitotic oligodendrocytes, notably olig1, Sox-10, Nkx2.2, Nkx6.2, Ying Yang 1, and ZFP488 [18][19][20][21][22][23] .…”

Section: Intrinsic Signalsmentioning

confidence: 99%

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Zhang

Guo

2013

Neurosci. Bull.

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Multiple sclerosis (MS) is a chronic and devastating autoimmune demyelinating disease of the central nervous system. With the increased understanding of the pathophysiology of this disease in the past two decades, many disease-modifying therapies that primarily target adaptive immunity have been shown to prevent exacerbations and new lesions in patients with relapsing-remitting MS. However, these therapies only have limited efficacy on the progression of disability. Increasing evidence has pointed to innate immunity, axonal damage and neuronal loss as important contributors to disease progression. Remyelination of denuded axons is considered an effective way to protect neurons from damage and to restore neuronal function. The identification of several key molecules and pathways controlling the differentiation of oligodendrocyte progenitor cells and myelination has yielded clues for the development of drug candidates that directly target remyelination and neuroprotection. The long-term efficacy of this strategy remains to be evaluated in clinical trials. Here, we provide an overview of current and emerging therapeutic concepts, with a focus on the opportunities and challenges for the remyelination approach to the treatment of MS.

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Common Developmental Requirement for Olig Function Indicates a Motor Neuron/Oligodendrocyte Connection

Cited by 962 publications

References 40 publications

BMP signaling mutant mice exhibit glial cell maturation defects

BMP signaling mutant mice exhibit glial cell maturation defects

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

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