Cell death and control of cell survival in the oligodendrocyte lineage

Barres, Ben A.; Hart, Ian; Coles, Harriet; Burne, Julia F.; Voyvodic, James T.; Richardson, William D.; Raff, Martin

doi:10.1016/0092-8674(92)90531-g

Cited by 1,265 publications

(1,011 citation statements)

References 95 publications

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“…PDGF has been shown to increase survival of O2-A cells in culture (Barres et al, 1992). In GFAP-expressing astrocytes autocrine PDGF stimulation was shown to induce dedifferentiation in vitro (Dai et al, 2001).…”

Section: Effect Of Oncogenic Pdgf-b Akt and K-ras Stimulation On Primentioning

confidence: 99%

Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma

et al. 2009

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Gliomas are primary brain tumors mainly affecting adults. The cellular origin is unknown. The recent identification of tumor-initiating cells in glioma, which share many similarities with normal neural stem cells, has suggested the cell of origin to be a transformed neural stem cell. In previous studies, using the RCAS/tv-a mouse model, platelet-derived growth factor B (PDGF-B)-induced gliomas have been generated from nestin or glial fibrillary acidic protein-expressing cells, markers of neural stem cells. To investigate if committed glial progenitor cells could be the cell of origin for glioma, we generated the Ctv-a mouse where tumor induction would be restricted to myelinating oligodendrocyte progenitor cells (OPCs) expressing 2 0 ,3 0 -cyclic nucleotide 3 0 -phosphodiesterase. We showed that PDGF-B transfer to OPCs could induce gliomas with an incidence of 33%. The majority of tumors resembled human WHO grade II oligodendroglioma based on close similarities in histopathology and expression of cellular markers. Thus, with the Ctv-a mouse we have showed that the cell of origin for glioma may be a committed glial progenitor cell.

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Section: Effect Of Oncogenic Pdgf-b Akt and K-ras Stimulation On Primentioning

confidence: 99%

Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma

et al. 2009

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“…Primary cultures of oligodendrocytes derived from the optic nerves of 12 day old Sprague-Dawley rats were obtained as described previously (Barres et al, 1992), with minor modifications (Alberdi et al, 2002). Cells were seeded into 24-well plates bearing 12-14-mm-diameter coverslips coated with poly-D-lysine (10 lg/ml) at a density of 10,000 cells/well and maintained at 37°C and 5% CO 2 in a chemically defined medium (Barres et al, 1992).…”

Section: Optic Nerve Culturesmentioning

confidence: 99%

“…Cells were seeded into 24-well plates bearing 12-14-mm-diameter coverslips coated with poly-D-lysine (10 lg/ml) at a density of 10,000 cells/well and maintained at 37°C and 5% CO 2 in a chemically defined medium (Barres et al, 1992). At 1-3 days in vitro, cultures were composed of at least 98% O4/GalC 1 cells, as determined by immunofluorescence labeling with a mouse IgG3 anti-galactocerebroside antibody (3 lg/ml; Boehringer-Mannheim, Germany); the majority of the very few remaining cells immunolabeled for GFAP (Z0334; Dakocitomation).…”

Section: Optic Nerve Culturesmentioning

confidence: 99%

Differential oxidative stress in oligodendrocytes and neurons after excitotoxic insults and protection by natural polyphenols

Ibarretxe

Sánchez‐Gómez

Campos-Esparza

et al. 2005

Glia

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Oligodendrocytes are vulnerable to overactivation of both their AMPA receptors and their high-and low-affinity kainate receptors. Depending on the intensity of the insult and the type of receptor activated, excitotoxic oligodendrocyte death mediated by these receptors has different characteristics. One important consequence at a cellular level is the ensuing oxidative stress, related to Ca 21 -dependent alterations in mitochondrial functioning. We observed that oxidative stress associated with selective AMPA receptor activation is much higher than that associated with the selective activation of high-and low-affinity kainate receptors. Moreover, excitotoxic insults generate more intense oxidative stress in oligodendrocytes than in cortical neurons, though similar alterations in [Ca 21 ] i and mitochondrial potential were observed in both cell types. Nanomolar concentrations of mangiferin and morin, two natural polyphenols with antioxidant properties, partially protect oligodendrocytes as well as cortical neurons from mild, but not intense, insults mediated by AMPA receptors. In addition to presenting oxygen radical scavenging activity, mangiferin and morin attenuate the intracellular Ca 21 overload subsequent to the activation of AMPA receptors, a mechanism that may contribute to their protective properties. The inclusion of these antioxidant agents in therapeutic strategies for the treatment of diseases in which oligodendrocyte as well as neuron loss occurs may prove to be beneficial.

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“…Cytological features of apoptosis have been described in both mature (Kerr et al, 1972;Wyllie et al, 1980;Arends and Wyllie, 1991;Fawcett, 1994) and embryonic (Barres et al, 1992;Raff et al, 1993;White, 1993;Coles et al, 1993) systems. Chromatin condenses in coneshaped piles (torroid bodies) along the inner margin of the cell nucleus and often the nucleus then fragments into membrane-bound vesicles (apoptotic bodies).…”

Section: Apoptosis In Myocytesmentioning

confidence: 99%

Muscle cell death during the development of head and neck muscles in the chick embryo

McClearn

Medville

Noden

1995

Developmental Dynamics

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Degenerating myofibers have been reported in the embryos and neonates of a number of birds and mammals, but neither the pervasiveness of the phenomenon nor the spatiotemporal patterns of degeneration has been examined in detail. Using transmission electron microscopy, we determined the patterns of muscle cell death in the chick biventer cervicis, a head extensor muscle. Cell death is most pronounced at incubation days 10 through 15, and occurs throughout the muscle. This is the period during which many myofiber clusters segregate into individual fibers, each with a separate basal lamina, and secondary myofibers become demarcated. Cells of largest diameter, presumably the primary myofibers, are preferentially affected. Degenerating cells exhibit a cohort of cytological features consistent with apoptosis, including the presence of dense, darkly-staining, hypercontracted myofibrils, misshapen nuclei with irregular chromatin condensations along the nuclear envelope, and scores of cytoplasmic vesicles and vacuoles. In cross section some large diameter muscle cells are characterized by sparse, flocculent cytoplasm that is devoid of myofibrils and organelles. Some show disintegrating cell membranes. In longitudinal section 200-300 pm long regions of hypercontracted myofibrils alternate with areas devoid of fibrils; this arrangement suggests that the myofibrils break into segments that are in register along one part of a muscle fiber and entirely absent from the adjacent length of fiber. We have observed similar patterns of muscle cell degeneration in the complexus, splenius cervicis, depressor mandibulae, and branchiomandibularis muscles. By day 18 of incubation most signs of degeneration are absent and by hatching (day 21) the muscle fibers all appear healthy. Many of these cytological changes in embryonic head muscle cells are characteristic of programmed cell death. We hypothesize that large-scale death of myocytes is a normal part of avian myogenesis and an important mechanism for affecting the transformation from embryonic to hatching muscle patterning. o 1995 Wiley-Liss, Inc.

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Cell death and control of cell survival in the oligodendrocyte lineage

Cited by 1,265 publications

References 95 publications

Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma

Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma

Differential oxidative stress in oligodendrocytes and neurons after excitotoxic insults and protection by natural polyphenols

Muscle cell death during the development of head and neck muscles in the chick embryo

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