Prostaglandins and epithelial response to injury

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.