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

FEBS Lett. 2004 Mar 12;561(1-3):122-6. doi: 10.1016/S0014-5793(04)00139-5.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aquaporins / biosynthesis
  • Chloride Channels / biosynthesis
  • Cholera Toxin / pharmacology*
  • Gene Expression Regulation / drug effects*
  • Glucose Transporter Type 1
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / 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


  • Aquaporins
  • Chloride Channels
  • ClC-2 chloride channels
  • Glucose Transporter Type 1
  • Ion Channels
  • Membrane Transport Proteins
  • Monosaccharide Transport Proteins
  • Slc2a1 protein, rat
  • aquaporin 8
  • cif nucleoside transporter
  • Cholera Toxin