Proliferation Rate of Oligodendrocytes in Culture Can Be Influenced by Extrinsic Factors

Bologa, Liane; Z’graggen, A.; Herschkowitz, N

doi:10.1159/000112329

Cited by 14 publications

(5 citation statements)

References 10 publications

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“…Double-label immunofluorescence of A, B, highly branched cell that is both A, GD3+ and B, GFAP+. x 590. cells have been eliminated by complement-dependent lysis (Bologa et al, 1984). Immature cells may also be the source of "transformed" lines established from neonatal CNS (Bressler et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

Differentiation of astrocytes and oligodendrocytes from germinal matrix cells in primary culture

Goldman¹,

Geier²,

Hirano³

1986

J. Neurosci.

140

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Primary cultures derived from neonatal rat forebrain grow almost entirely as glial cultures, with a large astrocytic preponderance and smaller numbers of oligodendrocytic cells. Although both astrocytic and oligodendrocytic characteristics are acquired in vitro, the origins of both types of glia in primary cultures have not been determined. We tested the hypothesis that glia differentiate in vitro from immature neuroectodermal cells by following the fate of germinal zone cells in primary cultures. A monoclonal antibody that binds GD3 ganglioside was used as a marker for cells of the subventricular zone (SVZ), since antibody binding in newborn rat forebrain could be detected by immunofluorescence only in the SVZ of newborn rats (Goldman et al., 1984). We followed the expression of glial fibrillary acidic protein (GFAP), an astrocytic marker; galactocerebroside (GC), an oligodendrocytic marker; and GD3 during the first several weeks of culture. Both GFAP and GC expression were first detected in cells that bound the GD3 antibody. Astrocytes developed during the first week in vitro; eventually, they lost the ability to bind the GD3 antibody and most became GD3-/GFAP+ cells. In high-density cultures, a population of small cells that resided on top of the astrocytic monolayer retained GD3 expression. GC-antibody binding was first observed in these cells of the upper layer, although it was not readily apparent until the second week of culture. Few GC+ cells were seen in cultures grown at low density, however.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Differentiation of astrocytes and oligodendrocytes from germinal matrix cells in primary culture

Goldman¹,

Geier²,

Hirano³

1986

J. Neurosci.

140

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“…These questions were addressed both in organotypic slice cultures in vitro and adult rats in vivo by interfering with lesion-induced microglial activation by using different immuno-modulators, such as transforming growth factor-β1 (TGF-β1) (22,23), AG126 (tyrphostin, inhibitor of tyrosine kinase) (24,25), and L-leucinemethyl-ester (LLME, lysosomotrophic; kills selectively mononuclear cells) (17,26). Further, we analyzed the potential role of astrocytes by abolishing these cells by using the specific toxin αamino adipic acid (αAAA, glutamate-homologue, Na + -dependent uptake by astroglia) (27,28), and of oligodendrocytes by their ablation by using complement-dependent antigalactocerebroside antibody-mediated cytotoxicity (29,30).…”

mentioning

confidence: 99%

Modification of microglia function protects from lesion‐induced neuronal alterations and promotes sprouting in the hippocampus

2003

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Primary neuronal destruction in the central nervous system triggers rapid changes in glial morphology and function, after which activated glial cells contribute to secondary neuronal changes. Here we show that, after entorhinal cortex lesion, activation of microglia, but not other glial cells, leads to massive secondary dendritic changes of deafferentiated hippocampal neurons. Blocking of microglial activation in vivo reduced this secondary neuronal damage and enhanced regenerative axonal sprouting. In contrast, abolishing astrocytes or oligodendroglia did not result in specific neuronal changes. Furthermore, primary damage leads to an interleukin 1beta up-regulation, which is attenuated by the immuno-modulator transforming growth factor beta1, whereas tumor necrosis factor alpha is not affected. Modification of microglial activity following denervation of the hippocampus protects neurons from secondary dendritic alterations and therefore enables their reinnervation. These data render activated microglia a putative therapeutic target during the course of axonal degeneration.

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“…Oligodendrocytes have been reported to be the second most vulnerable brain cell type to injury after neurons (Dudley 1982). There is some evidence that this cell type is capable of reproducing following injury (Bologa et al 1984;Ludwin 1984), but the proliferative activity may occur some distance from the necrotic area (Persson 1976).…”

Section: Discussionmentioning

confidence: 99%

Cell proliferation after ischemic injury in gerbil brain

1985

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Tritiated thymidine autoradiography was used to measure cellular proliferation after ischemic injury in gerbil brain. Gerbils were subjected to bilateral occlusion of the common carotid arteries which resulted in areas of necrosis, or infarcts, in the posterior thalamus or midbrain. From 12 h to 10 days following the ischemia, gerbils were injected with 3H thymidine, sacrificed 4 h later, and the brains sectioned. In order to identify astrocytes and monocytes/macrophages, immunocytochemistry was performed prior to autoradiography, using antisera against glial fibrillary acidic protein and endothelial-monocyte reticuloendothelial antigen, respectively. Immunocytochemistry was also used to visualize microvessel laminin, myelin, and leakage of serum albumin. Lastly, a histochemical procedure for acid phosphatase activity was employed to verify cellular phagocytic activity in the wound. A reproducible sequence of reactions took place during the first 10 days after ischemia. Early changes included leakage of albumin and myelin breakdown, followed by arrival of monocytes at 2 days and their differentiation into macrophages by 5 days. These cells exhibited intense proliferation from 2 to 6 days post-ischemia. Microvessel endothelial cells were maximally labeled at 4 days post-ischemia. Hypertrophied astrocytes were apparent at 2 days and proliferated from 3 to 7 days post-ischemia, and by 10 days the wound was replaced by a "glial scar".

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Proliferation Rate of Oligodendrocytes in Culture Can Be Influenced by Extrinsic Factors

Cited by 14 publications

References 10 publications

Differentiation of astrocytes and oligodendrocytes from germinal matrix cells in primary culture

Differentiation of astrocytes and oligodendrocytes from germinal matrix cells in primary culture

Modification of microglia function protects from lesion‐induced neuronal alterations and promotes sprouting in the hippocampus

Cell proliferation after ischemic injury in gerbil brain

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