A Review of Prostanoid Receptors: Expression, Characterization, Regulation, and Mechanism of Action

Abstract

Prostaglandin signaling controls a wide range of biological processes from blood pressure homeostasis to inflammation and resolution thereof to the perception of pain to cell survival. Disruption of normal prostanoid signaling is implicated in numerous disease states. Prostaglandin signaling is facilitated by G-protein-coupled, prostanoid-specific receptors and the array of associated G-proteins. This review focuses on the expression, characterization, regulation, and mechanism of action of prostanoid receptors with particular emphasis on human isoforms.

Keywords: G-protein; eicosanoid; prostaglandin; prostanoid; receptor; signaling.

Fig. 1

Prostanoid metabolic pathway. Gene designations are given for the participating enzymes (rounded boxes), accepted acronyms given for metabolites (ovals), and accepted acronyms for receptors (grey boxes). Receptor binding only indicated for metabolites with an EC₅₀ in the nM range. Enzymes: AKR1B1, aldo-keto reductase 1B1; AKR1C3, aldo-keto reductase 1C3; CBR1, carbonyl reductase 1; FAM213B, prostamide/prostaglandin F synthase; HPGDS, Hematopoietic prostaglandin D synthase; HSA, human serum albumin; PTGDS, prostaglandin D₂ synthase; PTGES, prostaglandin E synthase; PTGES2, prostaglandin E synthase-2; PTGES3, prostaglandin E synthase-3; PTGIS, prostacyclin (PGI₂) synthase; PTGS1, Prostaglandin G/H Synthase 1; PTGS2, Prostaglandin G/H Synthase 2; TBXAS1, Thromboxane A Synthase 1. Note: Figure 1 is in color