Prostaglandin E2 (PGE2) is involved in a number of physiological and pathophysiological events in many tissues throughout the body¹. The physiological actions of PGE2 are mediated through its interaction with cell surface prostaglandin E receptors.

There are three pharmacologically defined subtypes of the EP receptor, EP1, EP2, and EP3, and these subtypes are suggested to be different in their signal transduction². These receptors belong to the G-protein coupled receptor (GPCR) superfamily. Like all members they have seven transmembrane domains with an extracellular N-terminal tail and an intracellular C-terminus. The EP2 receptor is expressed in the vasculature, the gastrointestinal tract, kidney and also in the ciliary muscles of the eye³.

PGE2 is known to play a central role in the pathophysiology of inflammation in synergy with other proinflammatory mediators. PGE2 inhibits the function and the proliferation of T cells and the histamine release from mast cells by increasing the intracellular level of cAMP⁴.

The EP2 subtype is thought to be in part responsible for vasodilation, oedema formation, hyperanalgesia, modulation of the immune system, and the breakdown of bone and cartilage associated with disorders such as rheumatoid arthritis⁵.