Introduction: Prostacyclin (PGI) is synthetized by PGI synthase (PGIS) and induces vasorelaxation via activation of cyclic AMP (cAMP) generating IP-receptor. Several components of the PGI signaling pathway are reduced in patients with pulmonary hypertension (PH).
Aim: To study the effect of 17β-estradiol (E2) on the PGI signaling pathway in human pulmonary arteries (HPA) and in their smooth muscle cells (hPASMC) derived from Group-3 PH and non-PH patients.
Methods: Following E2-treatments of isolated HPA and cultured hPASMC, we measured: 6-keto-Prostaglandin F (PGI stable metabolite) by ELISA, PGIS and IP protein levels by Western blot and HPA vasorelaxations with an organ bath system.
Results: Incubation with E2 (24/48 h, doses ≥ 10 nM) significantly increased the expression of PGIS in hPASMC derived from both PH (65-98%) and non-PH (21-33%) patients, whereas incubation with E2 (2 h, 0.1 and 1 µM) increased 6-keto-PGF production in HPA from Group-3 PH patients only, and did not affect 6-keto-PGF production in hPASMC from either non-PH or Group-3 PH patients. Increases in IP receptor expression were observed following 10 mM E2-treatment of hPASMC from non-PH (33% after 48 h) and Group-3 PH (23% after 24 h) patient lungs. Finally, preincubation with 100 nM E2 significantly increased arachidonic acid-induced vasorelaxation of HPA from non-PH patient lungs but not of HPA from Group-3 PH patient lungs.
Conclusion: E2-treatment may help to restore the PGI-pathway in Group-3 PH.
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