Abstract
When porcine endothelial cells were exposed to hypertonicity, both the level of ATA2 (amino acid transporter 2) mRNA and activity of amino acid transport System A increased transiently, peaking after about 6 and 9 h, respectively. Cycloheximide, like actinomycin D, prevented both responses, showing that an earlier step also involves protein synthesis. Withdrawal of hypertonicity after 6 h increased the rate of down regulation. These findings confirm that ATA2 is a major isoform of System A and show that changes in the expression of ATA2 mRNA precede both the induction and subsequent down regulation of transport activity.
Copyright 2001 Academic Press.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Transport System A*
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Amino Acids / metabolism*
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Animals
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Biological Transport / physiology
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cells, Cultured
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Cycloheximide / pharmacology
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Dactinomycin / pharmacology
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Endothelium, Vascular / cytology
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism*
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Hypertonic Solutions / pharmacology
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Nucleic Acid Synthesis Inhibitors / pharmacology
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Protein Synthesis Inhibitors / pharmacology
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RNA, Messenger / metabolism*
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Swine
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Transfection
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Water-Electrolyte Balance / drug effects
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Water-Electrolyte Balance / physiology*
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beta-Alanine / analogs & derivatives*
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beta-Alanine / pharmacokinetics
Substances
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Amino Acid Transport System A
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Amino Acids
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Carrier Proteins
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Hypertonic Solutions
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Membrane Proteins
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Nucleic Acid Synthesis Inhibitors
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Protein Synthesis Inhibitors
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RNA, Messenger
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beta-Alanine
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2,2-dimethyl-beta-alanine
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Dactinomycin
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Cycloheximide