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Articles in PresS, published online ahead of print November 13, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00240.2002
Submitted on June 20, 2002
Accepted on November 6, 2002
1 Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: chouchen{at}im.wustl.edu.
The biological activities of prostaglandin E2 (PGE2) are mediated through EP receptors (EP1- EP4), plasma membrane G-protein coupled receptors, which differ in ligand binding and signal transduction pathways. We investigated gastrointestinal EP2 receptor expression in adult mice before and after radiation injury; and evaluated intestinal stem cell survival and crypt epithelial apoptosis following radiation injury in EP2 null mice. Results: EP2 was expressed throughout the gut. Intestinal EP2 mRNA increased 5-fold after 
- irradiation. Crypt survival was diminished in EP2-/- mice (4.06 crypts / cross section) compared with wild-type littermates (8.15 crypts/cross section). Radiation-induced apoptosis was significantly increased in EP2-/- mice compared with wild-type littermates. Apoptosis was 1.6 fold higher in EP2-/- mice (5.9 apoptotic cells/crypt) than in wild-type mice (3.5-apoptotic cells/crypt). Conclusions: The EP2 receptor is expressed in mouse gastrointestinal epithelial cells and is upregulated following radiation injury. The effects of PGE2 on both crypt epithelial apoptosis and intestinal crypt stem cell survival are mediated through the EP2 receptor.
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