Abstract
ICAM-1 is a cell surface adhesion glycoprotein playing an essential role in inflammatory responses. We have investigated the effects of the thyroid hormone T3 on the expression of the ICAM-1 gene in C6 glioma cells. In these cells, T3 stimulated the ICAM-1 protein expression significantly after 24 h of treatment. The induction of ICAM-1 by cytokines such as interleukin 1beta or tumour necrosis factor TNF as well as by lipopolysaccharide or T3 can be suppressed by the two anti-inflammatory compounds dexamethasone and parthenolide. The C6 glioma cell line could then be a useful model for studying the effect of T3 hormone on the expression of specific genes in glial cells, especially genes involved in lymphocyte-glial cell interactions.
MeSH terms
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Actins / metabolism
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Animals
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Blood-Brain Barrier / drug effects*
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Blood-Brain Barrier / physiology
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Cell Division / drug effects
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Cell Division / physiology
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Dexamethasone / pharmacology
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Encephalitis / metabolism*
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Encephalitis / pathology
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Encephalitis / physiopathology
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Gene Expression Regulation, Neoplastic / drug effects
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Gene Expression Regulation, Neoplastic / physiology
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Glial Fibrillary Acidic Protein / metabolism
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Glioma
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Intercellular Adhesion Molecule-1 / biosynthesis
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Intercellular Adhesion Molecule-1 / drug effects*
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Interleukin-1 / pharmacology
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Lipopolysaccharides / pharmacology
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Models, Animal
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Neuroglia / cytology
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Neuroglia / drug effects*
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Neuroglia / metabolism
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Rats
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Sesquiterpenes / pharmacology
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Triiodothyronine / metabolism
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Triiodothyronine / pharmacology*
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Tumor Cells, Cultured / cytology
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Tumor Cells, Cultured / drug effects*
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Tumor Cells, Cultured / metabolism
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Tumor Necrosis Factor-alpha / pharmacology
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Up-Regulation / drug effects
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Up-Regulation / physiology
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Vimentin / metabolism
Substances
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Actins
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Glial Fibrillary Acidic Protein
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Interleukin-1
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Lipopolysaccharides
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Sesquiterpenes
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Tumor Necrosis Factor-alpha
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Vimentin
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Triiodothyronine
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Intercellular Adhesion Molecule-1
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parthenolide
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Dexamethasone