Two proliferative stages of the oligodendrocyte lineage (A2B5+O4- and O4+GaIC-) under different mitogenic control

Gard, Anthony L.; Pfeiffer, S. E.

doi:10.1016/0896-6273(90)90216-3

Cited by 272 publications

(190 citation statements)

References 65 publications

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“…Oligodendrocyte precursors develop through a series of stages that have been characterized by their distinct cell morphology and the expression of cell surface proteins: the migratory OPC is typically a PSA-NCAM-positive cell that also expresses a ganglioside recognized by the A2B5 antibody (Gard and Pfeiffer, 1990;Shi et al, 1998). These precursor cells are extremely dependent on the presence of PDGF for proliferation and can be identified because they express high levels of the PDGF receptor (Baron et al, 2002;Barres et al, 1992) while surrounding neurons secrete PDGF (Ellison et al, 1996).…”

Section: Oligodendrocytes Developmentmentioning

confidence: 99%

Glial cells: Old cells with new twists

Ndubaku

Bellard

2008

Acta Histochemica

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SummaryBased on their characteristics and function -migration, neural protection, proliferation, axonal guidance and trophic effects -glial cells may be regarded as probably the most versatile cells in our body. For many years, these cells were considered as simply support cells for neurons. Recently, it has been shown that they are more versatile than previously believed -as true stem cells in the nervous system -and are important players in neural function and development. There are several glial cell types in the nervous system: the two most abundant are oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Although both of these cells are responsible for myelination, their developmental origins are quite different. Oligodendrocytes originate from small niche populations from different regions of the central nervous system, while Schwann cells develop from a stem cell population (the neural crest) that gives rise to many cell derivatives besides glia and which is a highly migratory group of cells.

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Section: Oligodendrocytes Developmentmentioning

confidence: 99%

Glial cells: Old cells with new twists

Ndubaku

Bellard

2008

Acta Histochemica

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“…Nestin was detected using anti-nestin monoclonal IgG1 (1:1 dilution; DSHB). Mouse anti-A2B5 IgM (1:200, Chemicon) was used to detect oligodendrocyte-type 2 astrocyte bipotent (O-2A) progenitors (Raff et al, 1983;Raff et al, 1984;Gard and Pfeiffer, 1990). In some instances, Hoechst 33342 (15 μg/ml in 0.1% BSA in PBS for 15 min at room temperature) was used to counterstain cell nuclei.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Glial-restricted precursors: Patterns of expression of opioid receptors and relationship to human immunodeficiency virus-1 Tat and morphine susceptibility in vitro

et al. 2007

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Recent evidence suggests that HIV-induced pathogenesis is exacerbated by opioid abuse and that the synergistic toxicity may result from direct actions of opioids in immature glia or glial precursors. To assess whether opioids and HIV proteins are directly toxic to glial-restricted precursors (GRPs), we isolated neural stem cells from the incipient spinal cord of embryonic day 10.5 ICR mice. GRPs were characterized immunocytochemically and by RTPCR. At 1 day in vitro (DIV), GRPs failed to express μ (MOR or MOP) or κ-opioid receptors (KOR or KOP); however, at 5 DIV, most GRPs expressed MOR and KOR. The effects of morphine (500 nM) and/or Tat (100 nM) on GRP viability were assessed in GRPs at 5 DIV by examining the apoptotic effector caspase-3 and cell viability (ethidium monoazide exclusion) at 96 h following continuous exposure. Tat or morphine alone or in combination caused significant increases in GRP cell death at 96 h, but not at 24 h, following exposure. Although morphine or Tat caused increases in caspase-3 activity at 4 h, this was not accompanied with increased cleaved caspase-3 immunoreactive or ethidium monoazide-positive dying cells at 24 h. The results indicate that prolonged morphine or Tat exposure is intrinsically toxic to isolated GRPs and/or their progeny in vitro. Moreover, MOR and KOR are widely expressed by Sox2 and/or Nkx2.2-positive GRPs in vitro and the pattern of receptor expression appears to be developmentally regulated. The temporal requirement for prolonged morphine and HIV-1 Tat exposure to evoke toxicity in glia may coincide with the attainment of a particular stage of maturation and/or the development of particular apoptotic effector pathways and may be unique to spinal cord GRPs. Should similar patterns occur in vivo then we predict that immature astroglia and oligodendroglia may be preferentially vulnerable to HIV-1 infection or chronic opiate exposure.

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“…Antibodies for glial lineage analysis included monoclonals A2B5 (Eisenbarth et al, 1979), O1 and 04 (Sommer and Scbachner, 1981), and RmAb (Ranscht et ~., 1982). A2B5 and 04 recognize surface antigens expressed during progdnitor cell maturation (Bansal et al, 1989;Dubois-Daleq, 1987;Gard and Pfeiffer, 1990). The O1 antibody is specific for the oligodendrocyte differentiation marker galactocerebroside (G-C) (Raft et al, 1978), while RmAb recognizes GC, sulfatide, and related glycolipids (Bansal et al, 1989).…”

Section: Immunocytochemistrymentioning

confidence: 99%