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

Abstract

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.