Astrocytes promote process outgrowth by adult human oligodendrocytes in vitro through interaction between bFGF and astrocyte extracellular matrix

Oh, Luke; Yong, V. Wee

doi:10.1002/(sici)1098-1136(199607)17:3<237::aid-glia6>3.0.co;2-y

Cited by 69 publications

(28 citation statements)

References 104 publications

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“…In this regard, astrocytes produce a range of neurotrophic factors and are conducive substrates for the growth of neurons in vitro and in vivo (Lindsay, 1979;Silver and Ogawa, 1983;Noble et al, 1984;Smith et al, 1986). We have found that astrocytes facilitate the extension of processes from the oligodendrocyte soma (Oh and Yong, 1996), an early event in myelinogenesis, and also protect oligodendrocytes against free radical-mediated damage (Noble et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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The relevance of astrogliosis remains controversial, especially with respect to the beneficial or detrimental influence of reactive astrocytes on CNS recovery. This dichotomy can be resolved if the mediators of astrogliosis are identified. We have measured the levels of transcripts encoding inflammatory cytokines in injury systems in which the presence or absence of astrogliosis could be produced selectively. A stab injury to the adult mouse brain using a piece of nitrocellulose (NC) membrane elicited a prompt and marked increase in levels of transcripts for interleukin (IL)-1α, IL-1β, and tumor necrosis factor (TNF)-α, which are considered to be microglia/macrophage cytokines. The elevations preceded, or occurred concomitantly with, the rise in glial fibrillary acidic protein mRNA, an early manifestation of astrogliosis. In neonatal mice, IL-1 and TNF-α mRNA were elevated to a greater extent by an NC-implant injury, which produced astrogliosis, than after an NC-stab, with minimal astrogliosis. We determined whether endogenous interferon (IFN)-γ could be responsible for the observed increases in IL-1 and TNF-α, because IFN-γ is a potent microglia/macrophage activator, and because its exogenous administration to rodents enhanced astrogliosis after adult or neonatal insults. A lack of requirement for endogenous IFN-γ was demonstrated by three lines of evidence. First, no increase in IFN-γ transcripts could be found at injury. Second, the administration of a neutralizing antibody to IFN-γ did not attenuate astrogliosis. Third, in IFN-γ knockout adult mice, astrogliosis and increases in levels of IL-1α and TNF-α were induced rapidly by injury. The marked elevation of inflammatory cytokines is discussed in the context of astrogliosis and general CNS recovery.

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Section: Discussionmentioning

confidence: 99%

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

et al. 1997

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“…Second, sulfatide carries a negative charge and can therefore bind to positively charged proteins by electrostatic forces, a characteristic that may account for the large number of sulfatide -protein interactions (for review, see Vos et al, 1994). Of particular interest is a well documented role for sulfatide, but not for GalC, in adhesion with extracellular matrix molecules, such as tenascin-R/janusin/J-1, laminin, and thrombospondin (Roberts and Ginsburg, 1988;Pesheva et al, 1997), that are present in the CNS (McLoon et al, 1988;O'Shea et al, 1990;Bartsch et al, 1992) and are secreted by the OLs and/or astrocytes in culture (Oh and Yong, 1996;Pesheva et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Negative Regulation of Oligodendrocyte Differentiation by Galactosphingolipids

1999

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Galactocerebroside and sulfatide, major galactosphingolipid components of oligodendrocyte plasma membranes and myelin, are first expressed at a critical point, when progenitors cease to proliferate and commence terminal differentiation. We showed previously that an antibody to galactocerebroside/ sulfatide arrested terminal differentiation, suggesting a role for these galactolipids in oligodendrocyte differentiation. We have now investigated the differentiation of oligodendrocytes (1) in response to other anti-galactolipid antibodies, showing that anti-sulfatide O4 but not anti-galactocerebroside O1 blocks terminal differentiation, perhaps by mimicking an endogenous ligand, and (2) in a transgenic mouse unable to synthesize these lipids because of mutation of the gene for ceramide galactosyltransferase, a key enzyme for galactosphingolipid synthesis. We find that galactosyltransferase mRNA expression begins at the late progenitor [pro-oligodendroblast (Pro-OL)] stage of the lineage and that the late progenitor marker prooligodendroblast antigen is not synthesized in the absence of galactosyltransferase. The principal outcome of the elimination of these galactolipids is a two-to threefold enhancement in the number of terminally differentiated oligodendrocytes both in culture and in vivo. Because the general pattern of differentiation and the level of progenitor proliferation and survival appear to be unaltered in the mutant cultures, we conclude that the increased number of oligodendrocytes is caused by an increased rate and probability of differentiation. In agreement with these two experimental approaches, we present a model in which galactosphingolipids (in particular galactocerebroside and/or sulfatide) act as sensors and/or transmitters of environmental information, interacting with endogenous ligands to function as negative regulators of oligodendrocyte differentiation, monitoring the timely progress of Pro-OLs into terminally differentiating, myelin-producing oligodendrocytes.

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“…In vitro experiments showed that astrocytes favor the migration of oligodendrocyte progenitors via adhesion molecules [148] and are required for the expression of maturation markers by oligodendrocyte lineages [149,150]. Myelinogenesis is facilitated in vitro by astrocytes [151], which also promote the outgrowth of oligodendrocyte processes [152] and the interaction between oligodendrocyte processes and axons, a crucial step in the initiation of myelination [153]. The experimental induction of demyelinating lesions in vivo proved the importance of astrocytic factors in remyelination [154 -156].…”

Section: Specific Astrocyte-oligodendrocyte Interactionsmentioning

confidence: 99%

Alexander disease: putative mechanisms of an astrocytic encephalopathy

Mignot

Boespflug‐Tanguy

Gelot

et al. 2004

CMLS, Cell. Mol. Life Sci.

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Alexander disease (AXD) is the first primary astrocytic disorder. This encephalopathy is caused by dominant mutations in the glial fibrillary acidic protein (GFAP) gene, encoding the main intermediate filament of astrocyte. Pathologically, this neurodegenerative disease is characterised by dystrophic astrocytes containing intermediate filament aggregates associated with myelin abnormalities. More than 20 GFAP mutations have been reported. Many of them cluster in highly conserved regions between several intermediate filaments. Contrary to other intermediate filament-related diseases, AXD seems to be the consequence of a toxic gain of function induced by aggregates. This is supported by the phenotype of mice overexpressing human GFAP. Nevertheless, GFAP null mice display myelin abnormalities and blood-brain barrier dysfunction that are present in AXD. Given the pivotal role of astrocytes in brain physiology, there are many possibilities for astrocytes to dysfunction and to impair the functions of other cells. Physiopathological hypotheses are discussed in the frame of AXD.

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Astrocytes promote process outgrowth by adult human oligodendrocytes in vitro through interaction between bFGF and astrocyte extracellular matrix

Cited by 69 publications

References 104 publications

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

Astrogliosis in the Neonatal and Adult Murine Brain Post-Trauma: Elevation of Inflammatory Cytokines and the Lack of Requirement for Endogenous Interferon-γ

Negative Regulation of Oligodendrocyte Differentiation by Galactosphingolipids

Alexander disease: putative mechanisms of an astrocytic encephalopathy

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