Epoprostenol is a synthetic analogue of the naturally occurring eicosanoid prostacyclin [1]. The inhibitory effect of epoprostenol on platelet aggregation is mediated by the stimulation of adenylate cyclase and the subsequent increase of cyclic adenosine monophosphate-3', 5' (cAMP) in platelets, leading to a rise in the intracellular levels of cyclic AMP [2]. Epoprostenol is widely used in studies on pulmonary arterial hypertension (PAH) to promote vascular dilation[3].
In vitro, Epoprostenol treatment for 24h at 1.0ng/ml induced apoptosis in PAH-pulmonary artery smooth muscle cells (PASMCs), resulting in increased cAMP levels and upregulated FasL expression[4].
References:
[1] Provencher S, Paruchuru P, Spezzi A, et al. Quality of life, safety and efficacy profile of thermostable flolan in pulmonary arterial hypertension[J]. PLoS One, 2015, 10(3): e0120657.
[2] Mohammadi A, Matos W F, Intriago C, et al. Use of Epoprostenol in the treatment of pulmonary arterial hypertension[J]. Cureus, 2021, 13(9).
[3] Sitbon O, Noordegraaf A V. Epoprostenol and pulmonary arterial hypertension: 20 years of clinical experience[J]. European Respiratory Review, 2017, 26(143).
[4] Akagi S, Nakamura K, Matsubara H, et al. Prostaglandin I2 induces apoptosis via upregulation of Fas ligand in pulmonary artery smooth muscle cells from patients with idiopathic pulmonary arterial hypertension[J]. International journal of cardiology, 2013, 165(3): 499-505.