Abstract
We investigate the role of β-catenin signaling in the response of macrophage to lipopolysaccharide (LPS) using RAW264.7 cells. LPS rapidly stimulated cytosolic β-catenin accumulation. β-catenin-mediated transcription was showed to be required for LPS induced gene expression and cell migration. Mechanically, ERK activation-primed GSK3β inactivation by Akt was demonstrated to mediate the LPS induced β-catenin accumulation. Overall, our findings suggest that suppression of GSK3β by ERK stimulates β-catenin signaling therefore contributes to LPS induced cell migration in macrophage activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Line
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Cell Movement / drug effects*
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Enzyme Activation / drug effects
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Extracellular Signal-Regulated MAP Kinases / metabolism*
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Gene Expression Regulation, Enzymologic / drug effects
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Glycogen Synthase Kinase 3 / metabolism*
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Glycogen Synthase Kinase 3 beta
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Lipopolysaccharides / pharmacology*
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Macrophages / cytology
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Macrophages / drug effects*
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Macrophages / enzymology
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Macrophages / metabolism
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Matrix Metalloproteinase 9 / genetics
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Mice
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction / drug effects*
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Transcription, Genetic / drug effects
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Wnt Proteins / metabolism
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beta Catenin / metabolism*
Substances
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Lipopolysaccharides
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Wnt Proteins
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beta Catenin
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Glycogen Synthase Kinase 3 beta
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Gsk3b protein, mouse
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Proto-Oncogene Proteins c-akt
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Extracellular Signal-Regulated MAP Kinases
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Glycogen Synthase Kinase 3
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Matrix Metalloproteinase 9