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Cholera toxin induces expression of ion channels and carriers in rat small intestinal mucosa.

Journal article
Authors Carl-Fredrik Flach
Stefan Lange
Eva Jennische
Ivar Lönnroth
Published in FEBS letters
Volume 561
Issue 1-3
Pages 122-6
ISSN 0014-5793
Publication year 2004
Published at Institute of Medical Microbiology/Immunology
Institute of Anatomy and Cell Biology
Institute of Laboratory Medicine, Dept of Clinical Bacteriology
Pages 122-6
Language en
Keywords Animals, Aquaporins, biosynthesis, Chloride Channels, biosynthesis, Cholera Toxin, pharmacology, Gene Expression Regulation, drug effects, Glucose Transporter Type 1, Intestinal Mucosa, cytology, drug effects, metabolism, Intestine, Small, cytology, Ion Channels, biosynthesis, Kinetics, Male, Membrane Transport Proteins, biosynthesis, Monosaccharide Transport Proteins, biosynthesis, Oligonucleotide Array Sequence Analysis, Rats, Rats, Sprague-Dawley
Subject categories Medical and Health Sciences


Cholera toxin causes cyclic adenosine monophosphate (cAMP)-induced electrolyte and water secretion in the small intestine. The toxin-induced change in gene expression in rat small intestine was evaluated with microarray technique and the results were confirmed by semiquantitative polymerase chain reaction (PCR). The transporter CNT2 for nucleosides was upregulated between 6 and 18 h after challenge, whereas the level of GLUT1 transporter for glucose became elevated at 6 h. Both changes probably facilitate uptake of these nutrients in the gut. At 18 h, the major chloride channel in the villus, ClC2, was upregulated. Aquaporin 8 was downregulated at 6 h and two mucin-producing genes were upregulated 18 h after toxin challenge. The expression was back to normal after 72 h, which is the turnover time for intestinal epithelial cells.

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