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Cholera toxin induces expression of ion channels and carriers in rat small intestinal mucosa
Author(s) -
Flach Carl-Fredrik,
Lange Stefan,
Jennische Eva,
Lönnroth Ivar
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(04)00139-5
Subject(s) - cholera toxin , glut1 , downregulation and upregulation , intestinal mucosa , small intestine , chemistry , toxin , microbiology and biotechnology , ion transporter , glucose transporter , biology , biochemistry , endocrinology , medicine , gene , insulin , membrane
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.