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  • 1
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In order to understand the molecular basis of the synergistic action of interferon γ (IFN-γ) and tumour necrosis factor α (TNF-α) on rat oligodendrocyte development, we studied some aspects of the signalling pathways involved in the regulation of the major histocompatibility complex (MHC) class I and the interferon regulatory factor 1 (IRF-1) gene expression. Two well-defined inducible enhancers of the MHC class I gene promoter, the MHC class I regulatory element (MHC-CRE) and the interferon consensus sequence (ICS), were analysed. Neither IFN-γ nor TNF-α was capable of inducing MHC-CRE binding activity when administrated alone. Following the exposure of oligodendrocytes to IFN-γ, TNF-R1 expression was transcriptionally induced by the binding of signal transducer and activator of transcription (STAT-1) homodimers to the IFN-γ activated site (GAS) present in the gene promoter. The upregulation of TNF-R1 allowed TNF-α to induce the binding of nuclear factor-κB (NF-κB) to the MHC-CRE site. With respect to ICS element, IFN-γ induced IRF-1 binding, that was further enhanced upon co-treatment with TNF-α. The existence of a synergism between IFN-γ and TNF-α in stimulating IRF-1 expression at the transcriptional level was supported by IRF-1 promoter analysis: IFN-γ directly induced the binding of STAT-1 homodimers to the GAS element, while NF-κB binding to the κB sequence was activated by TNF-α only after IFN-γ treatment. This transcriptional regulation of IRF-1 gene by IFN-γ and TNF-α was confirmed at the mRNA level. The synergism demonstrated in the present study highlights the importance of cytokine interactions in magnifying their biological effects during brain injury and inflammation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0012-1606
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Cell Biology International Reports 14 (1990), S. 47 
    ISSN: 0309-1651
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cytotechnology 5 (1991), S. 158-161 
    ISSN: 1573-0778
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract The aim of the present study was to understand the role of cellular interactions in the choice of the oligodendroglial differentiation route by bipotential progenitors (O-2A progenitors) of oligodendrocytes (OL) and type-2 astrocytes (AS). Cell populations enriched in 0-2A progenitors, obtained from mixed rat cortical glial cultures, were subcultured at low density in BME+10% fetal calf serum on a poly-L-lysine (PLL) substrate (controls) or on a substrate of purified type-1 AS killed by air drying (K-AS), in order to study the interactions between the two cell types independently of the soluble mitogen(s) secreted by type-1 AS. While on PLL the progenitors differentiated into type-2 AS within a week, on K-AS many of them differentiated into OL. However, on K-AS O-2A progenitors proliferated more than on PLL, and this proliferation appeared to be related to unknown polypeptide components of the extracellular matrix produced by type-1 AS. The preferential differentiation of O-2A progenitors into OL on K-AS may thus be partly related to the higher density achieved by the cells on this substrate. This hypothesis is supported by the observation that purified O-2A progenitors subcultured at high density on PLL largely differentiated into OL. The effect of cell density on lineage decision appeared to be related to the secretion of high molecular weight autocrine differentiation factors by O-2A lineage cells.
    Type of Medium: Electronic Resource
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