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Curr Opin Gastroenterol. 2007 Mar;23(2):107-10.

Prostaglandins and epithelial response to injury.

Author information

1
Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri 63110, USA. WStenson@im.wustl.edu

Abstract

PURPOSE OF REVIEW:

This review will highlight recent studies in the role of prostaglandins in regulating the epithelial response to injury in the gastrointestinal tract.

RECENT FINDINGS:

Prostaglandins, particularly PGE2, regulate intestinal epithelial apoptosis and proliferation in the face of injury. In the dextran sodium sulphate colitis model, PGE2, produced through cyclooxygenase-2, supports epithelial proliferation. Two studies demonstrated that PGE2 is an important mediator of the protective effects of toll-like receptor signaling in the dextran sulphate sodium model. One study suggested that toll-like receptor signaling induced cyclooxygenase-2 expression whereas the other suggested that toll-like receptor signaling induces the repositioning of cyclooxygenase-2 expressing stromal cells. PGE2 is also protective of small intestinal epithelial cells in the radiation injury model. In this model PGE2 decreases radiation-induced apoptosis and increases crypt survival. PGE2 binds to EP receptors; EP2 appears to be especially important in mediating the protective effects of PGE2 on epithelial cells. The intracellular signaling pathways by which PGE2 mediates its pro-proliferative and antiapoptotic effects include the PI3 kinase/Akt pathway, the MAP kinase pathway and the beta-catenin pathway.

SUMMARY:

Endogenous PGE2 has pro-proliferative and antiapoptotic effects on epithelial cells in gastrointestinal injury.

PMID:
17268236
DOI:
10.1097/MOG.0b013e3280143cb6
[Indexed for MEDLINE]
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