Here, we examined collagen and α-smooth muscle actin (α-SMA) expression in the fibrotic right ventricles of MCT-induced PAH rats with or without treatment with an EP4-specific agonist, L-902,688, as well as the effect of L-902,688 treatment on TGF-β-induced EndMT, which is characterized by a loss of endothelial cell markers (eNOS, E-cadherin, and CD146) and an increase in mesenchymal and EndMT markers (Twist and α-SMA). The gene discussed is ACTA1; the disease is pulmonary arterial hypertension.