Abstract
We examined the effect of lipopolysaccharide (LPS) or lipotechoic acid (LTA) on the regulation of hypoxia inducible factor (HIF-1) alpha on the MO3.13 cells, a human oligodendroglial cell line. Our study shows that MO3.13 cells express the toll like receptors (TLR's) but do not increase cellular levels of HIF-1 alpha following exposure to bacterial cell wall products. When MO3.13 cells were preconditioned by desferrioxamine (DFO) or cobalt chloride (CoCl(2)) and then treated with either LPS or LTA, HIF-1 alpha levels were higher than that induced by DFO or CoCl(2) alone. The increase in HIF-1 alpha was due to increased protein stability that was mediated by activation of the ERK-MAP kinase pathway.
MeSH terms
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Antimutagenic Agents / pharmacology*
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Bacteria / cytology
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Cell Line, Transformed
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Cell Wall / chemistry
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Cobalt / pharmacology*
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Deferoxamine / pharmacology*
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Dose-Response Relationship, Drug
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Drug Interactions
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Gene Expression Regulation / drug effects*
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / genetics
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
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Lipopolysaccharides / pharmacology
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Oligodendroglia / drug effects*
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Siderophores / pharmacology*
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Teichoic Acids / pharmacology
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Time Factors
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Toll-Like Receptors / genetics
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Toll-Like Receptors / metabolism
Substances
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Antimutagenic Agents
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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Lipopolysaccharides
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Siderophores
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Teichoic Acids
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Toll-Like Receptors
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Cobalt
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lipoteichoic acid
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cobaltous chloride
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Deferoxamine