Pulmonary arterial hypertension (PAH) is a severe and progressive disease, which is commonly associated with chronic hypoxemia in disorders such as chronic obstructive pulmonary disease.Prostacyclin analogs are widely used in the management of PAH patients.However, clinical efficacy and long-term tolerability of the prostacyclin analogs may be compromised by concomitant activation of other PG receptors, such as the E-prostanoid 3 receptor (EP3).Here, we found EP3 expression was up-regulated in both human and mouse pulmonary arterial vascular smooth muscle cells (PASMCs) in response to hypoxia, and in pulmonary arteries (PAs) from experimental PAH rodent models.