International Journal of Molecular Sciences Article Prostanoid EP2 Receptors Are Up-Regulated in Human Pulmonary Arterial Hypertension: A Key Anti-Proliferative Target for Treprostinil in Smooth Muscle Cells Jigisha A. Patel 1, Lei Shen 1, Susan M. Hall 2, Chabha Benyahia 3, Xavier Norel 3 ID , Robin J. McAnulty 4, Shahin Moledina 5, Adam M. Silverstein 6, Brendan J. Whittle 7 and Lucie H. Clapp 1,* ID 1 Institute of Cardiovascular Science, University College London, London WC1E 6JF, UK;
[email protected] (J.A.P.);
[email protected] (L.S.) 2 Infectious Diseases and Immunity, University College London, London WC1N 1EH, UK;
[email protected] 3 INSERM U1148, CHU X. Bichat, Paris Cedex 18, 75877 Paris, France;
[email protected] (C.B.);
[email protected] (X.N.) 4 Respiratory Centre for Inflammation and Tissue Repair, University College London, London WC1E 6JF, UK;
[email protected] 5 Paediatric Cardiology, Great Ormond Street Hospital, London WC1N 3JH, UK;
[email protected] 6 United Therapeutics Corporation, Research Triangle Park, NC 27709, USA;
[email protected] 7 William Harvey Research Institute, Queen Mary University of London, London EC1M 6BQ, UK;
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[email protected]; Tel.: +44-207-679-6180 Received: 18 July 2018; Accepted: 9 August 2018; Published: 12 August 2018 Abstract: Prostacyclins are extensively used to treat pulmonary arterial hypertension (PAH), a life-threatening disease involving the progressive thickening of small pulmonary arteries. Although these agents are considered to act therapeutically via the prostanoid IP receptor, treprostinil is the only prostacyclin mimetic that potently binds to the prostanoid EP2 receptor, the role of which is unknown in PAH.