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Prostacyclin receptor agonists induce DUSP1 to inhibit pulmonary artery smooth muscle cell proliferation.

par Maruyama, Hidekazu;Sakai, Satoshi;Dewachter, Laurence ;Dewachter, Céline ;Rondelet, Benoît ;Naeije, Robert ;Ieda, Masaki
Référence Life sciences, 315, page (121372)
Publication Publié, 2023-01

Article révisé par les pairs

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Résumé :

Upregulated p38MAPK signaling is implicated in the accelerated proliferation of pulmonary artery smooth muscle cells (PA-SMCs) and the pathogenesis of pulmonary artery remodeling observed in pulmonary arterial hypertension (PAH). Previously, we reported that after endothelin-1 (ET-1) pretreatment, bone morphogenetic protein 2 (BMP2) activates p38MAPK signaling and accelerates PA-SMC proliferation. The activity of p38MAPK signaling is tightly regulated by the inactivation of dual-specificity phosphatase 1 (DUSP1). Activated p38MAPK induces DUSP1 expression, forming a negative feedback loop. Prostacyclin IP receptor agonists (prostacyclin and selexipag) are used to treat PAH. In this study, we aimed to verify whether IP receptor agonists affect DUSP1 expression and accelerate the proliferation of PA-SMCs.