The trefoil gene family of mucus cell–secreted proteins is a critical mediator of gastrointestinal mucosal restitution. Transcription of trefoil genes is induced during mucosal repair, but the regulatory mechanisms involved are unknown. Mice deficient in the intestine-specific peptide intestinal trefoil factor (ITF), in which colonic restitution is lethally impaired, showed reduced expression of the gastric trefoil genes SP and pS2, suggesting that trefoil peptides may individually regulate transcription of the entire family. In gastric cell lines, the trefoils were shown to act in a manner suggestive of immediate-early genes capable of auto- and cross-induction through cis-acting regulatory regions. Trefoil-mediated transcriptional regulation required activation of the Ras/MEK/MAP kinase signal transduction pathway. EGF receptor (EGF-R) activation was also necessary for trefoil auto- and cross-induction, and both spasmolytic polypeptide (SP) and ITF stimulation of gastric cell lines led to phosphorylation of EGF-R. Nevertheless, ITF and ITF-thioredoxin cell surface binding at 4°C colocalized not with EGF-R, but with CD71, which is found in clathrin-coated pits, suggesting that integration of trefoil peptide responses may occur after internalization. As EGF-R expression is itself strongly induced after mucosal damage, the trefoil/EGF-R relationship may be pivotal in the generation and maintenance of the mucosal repair phenotype.
Douglas Taupin, Deng-Chyang Wu, Woo-Kyu Jeon, Kathryn Devaney, Timothy C. Wang, Daniel K. Podolsky
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Gastroenterology | 2006 |
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Peptides | 2006 |
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Alimentary Pharmacology & Therapeutics Symposium Series | 2006 |
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American journal of physiology. Cell physiology | 2005 |
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Digestive Diseases and Sciences | 2005 |
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American journal of physiology. Cell physiology | 2005 |
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Equine Internal Medicine | 2004 |
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Peptides | 2004 |
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Peptides | 2004 |
Disorders of the Gastrointestinal System
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Nature Reviews Molecular Cell Biology | 2003 |
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Transcriptional regulation of the human trefoil factor, TFF1, by gastrin1 1The authors thank Dr. Kazunari Yokoyama for providing the MAZ antibody, Dr. Marie-Christine Rio for the TFF1 antibody, Professor Sue Watson for the gastrin/CCKBR antibody, Professor Andrea Varro for the AGS-GR cells, and Dr. D. K. Podolsky for the TFF3 construct as well as Ian McEvoy for skilled technical assistance
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