Oligodendrocyte Precursor Cells from Different Brain Regions Express Divergent Properties Consistent with the Differing Time Courses of Myelination in These Regions

Power, Jennifer; Mayer-Pröschel, Margot; Smith, Joel; Noble, Mark

doi:10.1006/dbio.2002.0610

Cited by 86 publications

(81 citation statements)

References 44 publications

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“…An alternative and not necessary exclusive explanation for the apparently opposing effect of iron deficiency on the oligodendrocyte population in spinal cord and corpus callosum could be a reflection of the presence of specific precursor cell subpopulations which exhibit a different sensitivity to iron depletion. It has been established that glial precursor cells isolated from various brain regions respond differently to cytokines in respect to proliferation and differentiation but have identical antigenic properties [Power et al, 2002]. In addition, we have shown previously that glial precursor cells isolated from postnatal tissue respond differently to iron than embryonic derived precursor cells [Morath and Mayer-Pröschel, 2001].…”

Section: Discussionmentioning

confidence: 99%

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

Morath

Mayer-Pröschel

2002

Dev Neurosci

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One of the hallmarks of the pathology of iron deficiency in children is neurological disabilities that are often associated with hypomyelination. It has been hypothesized that this amyelination is mainly due to a disruption of myelin generation during the early postnatal stages when oligodendrocytes mature to generate myelin producing cell. In addition to these suggestions, we have previously provided in vitro data showing that iron affects both the proliferation and differentiation of glial precursor cells leading to a disruption in the generation of oligodendrocytes. We now present evidence demonstrating in vivo that iron deficiency during pregnancy affects the iron levels of various brain tissues in the developing fetus and disrupts not only the proliferation of their glial precursor cells but also disturbs the generation of oligodendrocytes from these precursor cells. In addition, we show that iron deficiency during embryogenesis affects glial lineage cells in a tissue-specific manner. Our studies offer the possibility to begin to comprehend whether any effects that occur during embryogenesis might have an influence on the establishment of the pathological defects that occur as a consequence of iron deficiency.

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Section: Discussionmentioning

confidence: 99%

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

Morath

Mayer-Pröschel

2002

Dev Neurosci

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“…[2][3][4][5] Multiple Sclerosis (MS) is the most common demyelinating disease of the CNS as well as one of the primary causes of neurological disability in young adults, and loss of oligodendrocytes at MS lesions has long been thought to be a primary contributor to disease. More recently, it has been found that oligodendrocytes are heterogeneous in nature 7 and that a significant number of OPCs migrate to and are present in MS lesions even in the chronic phases. If these endogenous cells could be stimulated to differentiate, this could represent a promising new therapeutic avenue for MS treatments.…”

Section: Introductionmentioning

confidence: 99%

High-Content Phenotypic Screening and Triaging Strategy to Identify Small Molecules Driving Oligodendrocyte Progenitor Cell Differentiation

Peppard

Rugg

Smicker³

et al. 2015

SLAS Discovery

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Multiple Sclerosis is a demyelinating disease of the CNS and the primary cause of neurological disability in young adults. Loss of myelinating oligodendrocytes leads to neuronal dysfunction and death and is an important contributing factor to this disease. Endogenous oligodendrocyte precursor cells (OPCs), which on differentiation are responsible for replacing myelin, are present in the adult CNS. As such, therapeutic agents that can stimulate OPCs to differentiate and remyelinate demyelinated axons under pathologic conditions may improve neuronal function and clinical outcome. We describe the details of an automated, cell-based, morphometric-based, high-content screen that is used to identify small molecules eliciting the differentiation of OPCs after 3 days. Primary screening was performed using rat CG-4 cells maintained in culture conditions that normally support a progenitor cell-like state. From a library of 73,000 diverse small molecules within the Sanofi collection, 342 compounds were identified that increased OPC morphological complexity as an indicator of oligodendrocyte maturation. Subsequent to the primary high-content screen, a suite of cellular assays was established that identified 22 nontoxic compounds that selectively stimulated primary rat OPCs but not C2C12 muscle cell differentiation. This rigorous triaging yielded several chemical series for further expansion and bio-or cheminformatics studies, and their compelling biological activity merits further investigation.

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“…The cortex develops later than the BF [18,26]. We considered the possibility that the lack of responsiveness to BDNF is due to the relative immaturity of the cortex.…”

Section: Bdnf Had No Effects On P14 Cortical Oligodendrocytesmentioning

confidence: 99%

“…It has been known for over seven decades that oligodendrocytes of different regions and within individual central nervous system (CNS) regions exhibit different morphologies [15]. Moreover, more recent studies indicate that oligodendrocyte populations differ in the expression of neurotransmitter receptors [16] as well as in response to specific growth factors [17,18].…”

Section: Introductionmentioning

confidence: 99%

Regionally Specific Effects of BDNF on Oligodendrocytes

et al. 2003

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To define the effects of neurotrophins on oligodendrocytes, we monitored NGF, BDNF and NT-3 actions on basal forebrain (BF) and cortical populations. NGF, BDNF and NT-3 applied to BF oligodendrocytes elicited increases in expression of myelin basic protein (MBP) and enhanced the numbers of MBP+ cells, without affecting total cell numbers. In the cortex, however, while NGF and NT-3 influenced MBP expression, BDNF was without effect. To explore this apparent regional difference in BDNF action, we compared expression of the neurotrophin receptors trkA, trkB and trkC. While BF cells expressed all three trks, cortical cells did not express the full-length BDNF receptor, trkB. Interestingly, in no case was any receptor expressed by all oligodendrocytes, indicating that oligodendrocytes may be heterogeneous within a brain region. The data suggest that BF oligodendrocytes are influenced by BDNF to express MBP and are distinct in this ability from cortical cells.

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Oligodendrocyte Precursor Cells from Different Brain Regions Express Divergent Properties Consistent with the Differing Time Courses of Myelination in These Regions

Cited by 86 publications

References 44 publications

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

Iron Deficiency during Embryogenesis and Consequences for Oligodendrocyte Generation in vivo

High-Content Phenotypic Screening and Triaging Strategy to Identify Small Molecules Driving Oligodendrocyte Progenitor Cell Differentiation

Regionally Specific Effects of BDNF on Oligodendrocytes

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