Background Endothelial cells, like gate-keepers of the vascular bed, can actively protect against the inflammatory process. Prostaglandin E2 (PGE2) could be one of the mediators that can promote the barrier function of endothelial cells. PGE2 exerts its cellular effects by binding to four different E-prostanoid receptors (EP1–4) that belong to the family of G protein-coupled receptors. This pro...

The closure time of the ductus arteriosus was investigated in 29 full term babies born vaginally after induction with prostaglandin E2 and in 22 controls. Serial Doppler echocardiography studies showed a significantly prolonged closure time in babies induced by prostaglandin E2. Whether the difference is related to changes in fetal prostaglandin E2 concentration remains to be established.

background: bone resorption is one of the main features of inflammatory periapical lesions and is mainly mediated by interleukin-1 beta (il-1β), tumor necrosis factoralpha (tnf-α) and prostaglandin-e2 (pge2). recent investigations of these lesions revealed that pharmacological modulation may be possible. objective: the aim of this study was to evaluate the effect of ibuprofen on il-1β, tnf-α an...

Prostaglandin E2 (PGE2) regulates membrane excitability, synaptic transmission, plasticity, and neuronal survival. The consequences of PGE2 release following seizures has been the subject of much study. Here we demonstrate that the prostaglandin E2 receptor 1 (EP1, or Ptger1) modulates native kainate receptors, a family of ionotropic glutamate receptors widely expressed throughout the central n...

Lipopolysaccharide is an inflammatory agent and interleukin-1 is a cytokine. Their pro-inflammatory effects may be mediated by prostanoids produced by inducible cyclooxygenase-2. The aim of this study was to determine the prostanoids produced by lipopolysaccharide and interleukin-1 stimulated enterocytes through the cyclooxygenase-1 and 2 pathways. Cultured enterocytes were stimulated with lipo...

High expression levels of cyclooxygenase 2 expression and infiltration by regulatory T cells (Tregs) are often associated with tumor progression. We have recently reported a prostaglandin E2 (PGE2)-dependent recruitment of Tregs to the tumor, suggesting that targeting specific PGE2 receptors may constitute a valuable approach to ablate the immuno-editing that occurs along with disease progression.