Abstract
The role of protein kinase C (PKC) in interleukin-1 beta- (II-1 beta)-, tumor necrosis factor-alpha- (TNF-alpha)-, and lipopolysaccharide- (LPS)-induced vascular cell adhesion molecule-1 (VCAM-1) expression on human umbilical vein endothelial cells (HUVEC) was studied. PKC inhibition or downregulation diminished VCAM-1 mRNA accumulation and protein expression. Interleukin-1 beta, TNF-alpha, and LPS induce nuclear factor (NF)-kappa B-like binding activity, which precedes VCAM-1 transcription. PKC inhibition did not prevent NF-kappa B-like binding activity, indicating that this is PKC-independent, and NF-kappa B-like binding activity is insufficient for transcription of VCAM-1.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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Cell Adhesion Molecules / genetics
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Cell Adhesion Molecules / metabolism*
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Cell Membrane / metabolism
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Cells, Cultured
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DNA-Binding Proteins / metabolism
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E-Selectin
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Endothelium, Vascular / metabolism*
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Enzyme Activation
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Gene Expression / drug effects
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Humans
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In Vitro Techniques
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Interleukin-1 / pharmacology
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Lipopolysaccharides / pharmacology
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Molecular Sequence Data
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NF-kappa B / metabolism
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Oligodeoxyribonucleotides / chemistry
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / physiology*
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RNA, Messenger / genetics
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Tetradecanoylphorbol Acetate / pharmacology
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Tumor Necrosis Factor-alpha / pharmacology
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Umbilical Veins
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Vascular Cell Adhesion Molecule-1
Substances
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Cell Adhesion Molecules
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DNA-Binding Proteins
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E-Selectin
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Interleukin-1
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Lipopolysaccharides
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NF-kappa B
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Oligodeoxyribonucleotides
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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Vascular Cell Adhesion Molecule-1
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Protein Kinase C
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Tetradecanoylphorbol Acetate