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STIMULATION OF STERIODOGENIC ACUTE REGULATORY PROTEIN mRNA EXPRESSION BY PROSTAGLANDIN E2 IN ENDOMETRIOTIC STROMAL CELLS.
Lin, Chen-Chung1, Wu, Meng-Hsing2, Tsai, Shaw-Jenq1, 1 2
ABSTRACT- This study determined the origin of prostaglandin E2 (PGE2), steroid hormones, and the regulation of enzymes participated in steroidogenic pathway in patients with endometriosis. Tissues and peritoneal fluids were collected from patients with endometriosis or other gynecological diseases at the time of lapaoratory or lapaoratomy at the National Cheng Kung University Hospital. Stromal cells were isolated from ectopic or eutopic endometrium. Progesterone (P4), estradiol (E2), and PGE2 concentrations were measured by ELISA, and mRNA concentrations were determined by SC-QC-RT-PCR. Eutopic and ectopic stromal cells were cultured and treated with IL-1
(0-100 ng/ml), TNF-
(0-100 pg/ml), or PGE2 (0-100 
M). Peritoneal fluid P4, E2, PGE2 concentrations were higher in women with endometriosis as compared to otherwise healthy women. Steroidogenic acute regulatory protein (StAR) mRNA was 10 times higher in endometriotic cells than that in normal endometrium. PGHS-2 mRNA was detected in eutopic endometrium, endometriotic lesions, and peritoneal macrophages of normal women and patients with endometriosis. On the other hand, peritoneal macrophages of normal women expressed higher concentration of PGHS-2 mRNA in per microgram DNA basis but the number of macrophages in peritoneal fluid was much greater in patients with endometriosis. Treatment of endometriotic stromal cells with PGE2 (10 nM) significantly increased StAR and PGHS-2 mRNA expression. Our results demonstrated that endometriotic lesions have steroidogenic capacity and PGE2 production ability. The locally produced PGE2 acts in a paracrine/autocrine fashion to upregulate enzymes that control the rate-limiting step of PGE2 and steroid production. This positive feedback action may play important roles in endometriosis formation.
KEY WORDS: endometriosis, PGHS-2, StAR, steroids