Differentiation of a medulloblastoma cell line towards an astrocytic lineage using the human T lymphotropic retrovirus-1

Giraudon, Pascale; Dufay, Nathalie; Hardin, Heather; Reboul, Ariel; Tardy, M.; Bein, Matthias

doi:10.1016/0306-4522(93)90553-r

Cited by 21 publications

(22 citation statements)

References 45 publications

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“…In previous studies we have established that Dev cells express neuronal and glial antigens when cultured in the medium containing high levels of fetal calf serum (Dufay et al, 1994;Giraudon et al, 1993). The expression of mature cell type-speci®c antigens such as neuro®laments, GFAP or galactocerebroside is not observed when Dev cells are plated and maintained in serum free medium (EA Derrington, C Bellin, N Dufay, A Jouvet, S Bertrand, G St-Pierre and M-F Belin, submitted).…”

Section: Dev Cells Express An Undi Erentiated Neuroepithelial Phenotymentioning

confidence: 99%

“…Previous investigations had suggested that Dev cells were capable of di erentiation towards either the astrocytic or neuronal pathways in response to exogenous stimuli (Dufay et al, 1994;Giraudon et al, 1993). The question of whether distinct subpopulations of cells within the cell line are responding was not addressed.…”

Section: Monoclonal Subclones Of the Dev Cell Linementioning

confidence: 99%

“…We have described a cell line, Dev, derived from a cerebellar PNET (medulloblastoma), which is unique among PNET cell lines because subpopulations of Dev cells can be induced to di erentiate towards neuronal or astrocytic lineages when they are cultivated in fetal calf serum (FCS) (Dufay et al, 1994;Giraudon et al, 1993). However, Dev cells are intrinsically undifferentiated in that they do not express mature neural markers when plated and maintained in the absence of FCS.…”

Section: Introductionmentioning

confidence: 99%

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Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Dufay

Rudkin

et al. 1998

Oncogene

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Primitive neuroectodermal tumours (PNET) are thought to derive from the malignant transformation of pluripotent CNS precursors although this hypothesis has yet to be tested in vitro. Here we show that cells of a human PNET cell line`Dev' express functional ®broblast growth factor (FGF) receptors (FGFR) and respond to FGF2 as multipotent CNS precursors. FGF2 induces tyrosine phosphorylation of FGFR-1 and FGFR-2 and many cellular substrates including MAP kinases and stimulates proliferation. Cells detach from plastic substrates and proliferate to form large clusters of undi erentiated cells. After adhesion to polylysine, cells migrate out from the clusters and di erentiate. The majority of di erentiated cells express neuronal phenotypes but distinct subpopulations express oligodendrocytic and astrocytic markers. Mature neural di erentiation markers are not otherwise detected in Dev cells in de®ned medium. Identical results were obtained with 12 monoclonal subclones as well as the parent cell line, con®rming that Dev cells are multipotent. This extends evidence that multipotent CNS precursors are the cellular substrate from which certain PNET develop and shows that FGF2 is a potent proliferation and di erentiation inducer for PNET cells in vitro, suggesting that FGF2 may also modulate the evolution of PNET in vivo. Finally our results suggest that PNET cell lines may provide models to elucidate the biology of human multipotent CNS precursors.

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Section: Dev Cells Express An Undi Erentiated Neuroepithelial Phenotymentioning

confidence: 99%

Section: Monoclonal Subclones Of the Dev Cell Linementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Dufay

Rudkin

et al. 1998

Oncogene

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“…It has long been suggested that viral infections might trigger an autoimmune response by several mechanisms including molecular mimicry (4,13). In the present study, we performed some experiments in order to document the existence of molecular mimicry of monoclonal antibodies and sera of TSP/HAM patients against several proteins of HTLV-I with proteins and subcellular structures of non-HTLV-I/HIV-1-infected primary cultured human astrocytes and other normal components of the CNS.…”

Section: Introductionmentioning

confidence: 97%

“…Previous studies have shown that astrocytes secrete inflammatory cytokines after transient contact with T cells persistently infected with HTLV-I (12). These in vitro-activated astrocytes may prolong and amplify the pathological effects produced by invading T cells, demonstrating the crucial role of astrocytes in brain homeostasis (13).…”

Section: Introductionmentioning

confidence: 99%

Autoimmunity and molecular mimicry in tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy

García-Vallejo

Domínguez

Tamayo

2005

Braz J Med Biol Res

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Viruses share antigenic sites with normal host cell components, a phenomenon known as molecular mimicry. It has long been suggested that viral infections might trigger an autoimmune response by several mechanisms including molecular mimicry. More than 600 antiviral monoclonal antibodies generated against 11 different viruses have been reported to react with 3.5% of cells specific for uninfected mouse organs. The main pathological feature of tropical spastic paraparesis/ human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (TSP/HAM) is a chronic inflammation of the spinal cord characterized by perivascular cuffing of mononuclear cells accompanied by parenchymal lymphocytic infiltration. We detected the presence of autoantibodies against a 98-to 100-kDa protein of in vitro cultured human astrocytes and a 33-to 35-kDa protein from normal human brain in the serum of HTLV-I-seropositive individuals. The two cell proteins exhibited molecular mimicry with HTLV-I gag and tax proteins in TSP/HAM patients, respectively. Furthermore, the location of 33-to 35-kDa protein cross-reaction correlated with the anatomical spinal cord areas (in the rat model) in which axonal damage has been reported in several cases of TSP/HAM patients. Our experimental evidence strongly suggests that the demyelinating process occurring in TSP/ HAM may be mediated by molecular mimicry between domains of some viral proteins and normal cellular targets of the spinal cord sections involved in the neurodegeneration.

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Changes in astrocytic glutamate catabolism enzymes following neuronal degeneration or viral infection

Belin

Didier-Bazes

Akaoka

et al. 1997

Glia

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Functional changes in astrocytes are among the earliest cellular responses to a wide variety of insults to the central nervous system (CNS). Such responses significantly contribute to maintaining CNS homeostasis. In this context, by controlling energetic metabolism and overall excitability of the CNS, the modulation of glutamate uptake and catabolism in astrocytes is crucial. Here, we review specific modulations of the expression of glutamate cabolizing enzymes (glutamate dehydrogenase and glutamine synthetase) in response to CNS insults (degeneration of serotonergic neurons or viral infection by a human retrovirus, HTLV‐I). The cellular and molecular mechanisms involved in the control of the glutamate catabolism are discussed in relation to neurological disorders. GLIA 21:154–161, 1997. © 1997 Wiley‐Liss, Inc.

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Differentiation of a medulloblastoma cell line towards an astrocytic lineage using the human T lymphotropic retrovirus-1

Cited by 21 publications

References 45 publications

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Autoimmunity and molecular mimicry in tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy

Changes in astrocytic glutamate catabolism enzymes following neuronal degeneration or viral infection

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