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

FEBS Letters

Jennische, Eva¹  Flach, Carl-Fredrik³  Lönnroth, Ivar³  Lange, Stefan² 

[1] Anatomy and Cell Biology, Box 420, Göteborg University, SE40530 Göteborg, Sweden;Clinical Bacteriology, Guldhedsgatan 10, 41346 Göteborg, Sweden;Medical Microbiology and Immunology, Box 435, SE40530 Göteborg, Sweden

关键词: Microarray;    Cholera toxin;    Gene expression;    Membrane transporter;    Mucin;    CT;    cholera toxin;    ClC2;    chloride channel 2;    GLUT;    glucose transporter;    CNT2;    concentrative nucleoside transporter 2;    AQP;    aquaporin;    MUC2;    mucin 2;    MUC3;    mucin 3;   

DOI  :  10.1016/S0014-5793(04)00139-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown