OBJECTIVE: To examine the regulation and the function of activin-A in stromal cells derived from endometrioma. DESIGN: Molecular studies. SETTING: University 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.
OBJECTIVE: To examine the regulation and the function of activin-A in stromal cells derived from endometrioma. DESIGN: Molecular studies. SETTING: University 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.