Activin-A is induced by interleukin-1β and tumor necrosis factor-α and enhances the mRNA expression of interleukin-6 and protease-activated receptor-2 and proliferation of stromal cells from endometrioma

ObjectiveTo examine the regulation and the function of activin-A in stromal cells derived from endometrioma.DesignMolecular studies.SettingUniversity research laboratory.Patient(s)Endometrioma stromal cells (EoSC) were obtained from 28 patients with ovarian endometrioma undergoing laparoscopy.Intervention(s)EoSC were cultured with inflammatory stimuli or recombinant activin-A, followed by RNA extraction.Main Outcome Measure(s)Activin mRNA expression was evaluated by real-time reverse transcription–polymerase chain reaction (RT-PCR), and activin-A concentration of supernatant of cultured EoSC was evaluated by ELISA. Also, the effect of activin-A on EoSC was evaluated with real-time RT-PCR and cell proliferation assay.Result(s)Inflammatory stimuli, interleukin (IL) -1β, and tumor necrosis factor (TNF) -α induced inhibin/activin-βA subunit mRNA and activin-A protein expression in EoSC. Additionally, activin-A enhanced EoSC proliferation and increased the expression of IL-6 and protease-activated receptor (PAR)-2 mRNA.Conclusion(s)An in vitro study revealed that activin-A, which is induced by IL-1β or TNF-α, might promote endometriosis by stimulating IL-6 and PAR-2 mRNA expression and increasing the proliferation of EoSC.