Abstract
Inflammation within the vasculature is associated with endothelial cell (EC) perturbation, loss of vascular ATP-diphosphohydrolase activity, and platelet microthrombus formation with release of ATP and ADP into the micro-environment. The nature and effects of purinergic stimulation of EC under these circumstances remain largely undetermined. ATP and ADP activated EC transcribed mRNA from certain transcription factor NF-kappa B target genes and expressed E-selectin protein on cell membranes. Band shift analysis and reporter assays confirmed the activation of NF-kappa B in response to both ATP and ADP. Apoptosis was shown to occur in response to purinergic signaling, potentially through the activation of P2z/P2x7 receptors. Induction of EC activation responses and apoptosis in response to stimulation with ATP and ADP is associated with activation of NF-kappa B.
MeSH terms
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Adenosine Diphosphate / pharmacology*
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Adenosine Triphosphate / pharmacology*
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Animals
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Aorta
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Apoptosis / drug effects*
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Cattle
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Cells, Cultured
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E-Selectin / biosynthesis*
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Endothelium, Vascular / cytology*
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / physiology*
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Genes, Reporter
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Mutagenesis, Site-Directed
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NF-kappa B / antagonists & inhibitors
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NF-kappa B / metabolism*
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Polymerase Chain Reaction
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Proto-Oncogene Proteins / biosynthesis
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Receptors, Purinergic / biosynthesis
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Recombinant Proteins / metabolism
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Swine
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Transcription Factor RelB
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Transcription Factors*
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Transcription, Genetic / drug effects
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Transcription, Genetic / physiology*
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Transfection
Substances
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E-Selectin
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NF-kappa B
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Proto-Oncogene Proteins
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Receptors, Purinergic
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Recombinant Proteins
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Transcription Factors
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Transcription Factor RelB
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Adenosine Diphosphate
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Adenosine Triphosphate