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Oligodendrocyte Progenitors (oligodendrocyte + progenitor)

Distribution by Scientific Domains
Medical Sciences50%
Life Sciences50%

Terms modified by Oligodendrocyte Progenitors

  • oligodendrocyte progenitor cell
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    Selected Abstracts

    Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS

    GLIA, Issue 7 2007
    Adam C. Vana
    Abstract Myelin transcription factor 1 (Myt1) is a zinc-finger DNA binding protein that influences developing oligodendrocyte progenitor (OP) cell proliferation, differentiation, and myelin gene transcription in vitro. The potential of Myt1 to play a role in OP responses leading to remyelination was examined using murine hepatitis virus strain A59 (MHV) to induce spinal cord demyelination and potential relevance to human pathology was evaluated in multiple sclerosis (MS) lesions. In MHV-infected mice, the density of Myt1 expressing cells markedly increased in lesioned areas of spinal cord white matter. Myt1 expressing cells proliferated most extensively during active demyelination and subsequently accumulated to maximal levels during early remyelination. Cells with nuclear Myt1 immunoreactivity were mainly OP cells, identified by co-localization with platelet-derived growth factor alpha receptor, with additional phenotypes being either oligodendrocytes or neural stem cells, identified by CC1 antigen and Musashi1, respectively. The density of OP cells expressing Myt1 was significantly increased in white matter of MHV-infected mice during demyelination and early remyelination then as remyelination advanced the values returned to levels comparable to PBS-injected control mice. In MHV lesions, Myt1 was not expressed in astrocytes, lymphocytes, or macrophage/microglial cells. MS lesions demonstrated increased Myt1 expression in both the periplaque white matter adjacent to lesions and within early remyelinating lesions. These results suggesta potential role for Myt1 in the regeneration of oligodendrocyte lineage cells in response to demyelination. © 2007 Wiley-Liss, Inc. [source]

    Regulation of SVZ-derived gliogenesis by inflammatory-demyelination

    JOURNAL OF NEUROCHEMISTRY, Issue 2002
    A. Baron-Van Evercooren
    Identifying a source of cells with the capacity to generate oligodendrocytes in the adult CNS would help the development of strategies to promote myelin repair. During development of the neonate rodent forebrain, most oligodendrocytes derive from the subventricular zone (SVZ), a germinative area which also contributes to the genesis of astrocytes and neurons. While the SVZ persists in the adult brain, its size is largely reduced and its contribution to cell genesis is essentially restricted to the renewal of the granular and periglomerular neurons of the olfactory bulb. Lesion derived signals can have a profound impact on the behavior of the SVZ cells. While cortical trauma triggers their mobilization and differentiation in astrocytes in the lesioned cortex (Holmin et al. 1997), focaly-induced demyelination promotes their migration in the demyelinated white matter and differentiation in astrocytes and oligodendrocytes (Nait-Oumesmar et al. 1999). Using EAE, we will show that multifocal demyelination (i) promotes the proliferation of the SVZ precursors (ii) enhances their migration towards the olfactory bulb and triggers their mobilization to multiple sites of the diseased white matter, and (iii) induces their differentiation in neurons, astrocytes and oligodendrocytes in the olfactory bulb, and in oligodendrocytes and astrocytes in the demyelinated white matter. SVZ precursors could thus be a source of oligodendrocytes and contribute with oligodendrocyte progenitors to the replacement of lost oligodendrocytes in demyelinating diseases of the adult CNS. [source]

    Abstinence From Moderate Alcohol Self-Administration Alters Progenitor Cell Proliferation and Differentiation in Multiple Brain Regions of Male and Female P Rats

    ALCOHOLISM, Issue 1 2009
    Jun He
    Background:, Acute and chronic ethanol exposure has been found to decrease hippocampal neurogenesis, reduce dendritic differentiation of new neurons, and increase cell death. Interestingly, abstinence from such treatment increases hippocampal neurogenesis and microglial genesis across several brain regions. The goal of the current investigation was to study cellular alterations on neuro- and cell-genesis during abstinence following alcohol self-administration using alcohol-preferring rats (P rats). Methods:, Male and female P rats were given the choice of drinking 10% alcohol in water or pure water for 7 weeks. Social interaction behavioral assessments were conducted at 5 hours upon removal of alcohol, followed by bromo-deoxyuridine (BrdU, 150 mg/kg × 1/d × 14 d) injections to label proliferating cells. Animals were then killed 4 weeks later to conduct immunohistochemical and confocal analyses using antibodies against BrdU and other phenotypic markers (NeuN for mature neurons; Iba-1 for microglia; GFAP for astrocytes; and NG2 for oligodendrocyte progenitors). Results:, Mild alcohol withdrawal anxiety was detected by reduction in social interactions. The number of hippocampal BrdU+ cells was increased approximately 50% during alcohol abstinence (26 ± 2.8 in controls vs. 39 ± 4 in alcohol group). BrdU+ cells were also increased in the substantia nigra (SN) approximately 65% in the alcohol abstinent group (12 ± 1 in controls vs. 19 ± 1.5 in alcohol group). No gender differences were found. Confocal analyses indicated that approximately 75% of co-localization of BrdU+ cells with NeuN in the hippocampal dentate gyrus (DG) resulting a net increase in neurogenesis in the alcohol abstinent group compared to controls. In cingulum, greater proportion of BrdU+ cells were co-localized with NG2 in the alcohol abstinent group indicating increased differentiation toward oligodendrocyte progenitors in both genders. However, the phenotype of the BrdU+ cells in SN and other brain regions were not identified by NeuN, Iba-1, GFAP, or NG2 suggesting that these BrdU+ cells probably remain in a nondifferentiated stage. Conclusions:, These data indicate that abstinence from moderate alcohol drinking increases hippocampal neurogenesis, cingulate NG2 differentiation, and SN undifferentiated cell proliferation in both males and females. Such cellular alteration during abstinence could contribute to the spontaneous partial restoration of cognitive deficits upon sobriety. [source]

    The age-related decrease in CNS remyelination efficiency is caused by an impairment of both oligodendrocyte progenitor recruitment and differentiation

    NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2002
    C. Zhao
    Developing strategies to reverse the age-associated decline in CNS remyelination requires the identification of how the regenerative process is impaired. We have addressed whether remyelination becomes slower because of an impairment of recruitment of oligodendrocyte progenitors (OPs) or, an impairment of OP differentiation into remyelinating oligodendrocytes. The OP response during remyelination of focal, toxin-induced CNS demyelination in young and old rats was compared by in situ hybridization using probes to PGDF-,R, and the OP transcription factor, MyT1. The expression patterns for both OP markers are very similar and reveal a delay in the colonization of the demyelinated focus with OPs in the old animals compared to young. By comparing the mRNA expression pattern MyT1 with that of the myelin proteins MBP and Gtx, we have found that in the old animals there is also a delay in OP differentiation, which increases with longer survival times. These results indicate that the age-associated decrease in remyelination efficiency occurs because of an impairment of OP recruitment and their subsequent differentiation into remyelinating oligodendrocytes, and that strategies aimed at ameliorating the age-associated decline in remyelination efficiency will therefore need to promote both components of the regenerative process. [source]