BACKGROUNDThe mechanisms of endometriosis with infertility have not been fully studied. The present study aimed to assess the follicular fluid (FF) levels of prostaglandin E2 (PGE2), which plays a critical role within the ovary, and to investigate the effect of PGE2 on steroidogenesis in granulosa-lutein cells (GLCs) from women with and without endometriosis.

METHODSThirty-three women with laparoscopically documented endometriosis and 40 controls undergoing in vitro fertilization (IVF) were studied. We assayed the concentrations of PGE2 in FF, the production of E2 and progesterone in FF and in culture medium, and the expression of steroidogenic acute regulatory protein (StAR) and CYP19A1 in GLCs with the intervention of PGE2.

RESULTSPGE2 and progesterone concentrations were increased and displayed positive correlation in endometriotic FF. PGE2 induced the expression of StAR and the production of progesterone in GLCs from women with endometriosis, and the expression of StAR and the production of progesterone were increased in GLCs from women with endometriosis. However, there were no significant effects of PGE2 on promoting the production of E2 or the expression of CYP19A1 in GLCs. Moreover, the production of E2 and the expression of CYP19A1 in GLCs from women with endometriosis were significantly decreased compared to the controls.

CONCLUSIONSPGE2 concentrations are increased in endometriotic FF, along with concomitant increases in progesterone and StAR. In contrast, the E2 and CYP19A1 are decreased in GLCs, which may delay the development of the follicles and cause an imbalance in the follicular steroid hormone levels. These changes may have close relationship with endometriosis-associated infertility.

Adult ; Dinoprostone ; metabolism ; Embryo Transfer ; Endometriosis ; metabolism ; Female ; Fertilization in Vitro ; Follicular Fluid ; metabolism ; Humans ; Luteal Cells ; Pregnancy

AIMTo study the effects of L-tyrosine on 3beta-HSD activity of rat luteal cells in vitro.

METHODSLuteal cells were isolated from ovary tissues of female rats pretreated with PMSG and hCG. Luteal cells were cultured with 95% oxygen and 5% carbon dioxide in 37 degrees C. 3beta-HSD activity was measured by radioimmunoassay (RIA).

RESULTS(1) 0.2 mmol x L(-1) and 2.0 mmol x L(-1) L-tyrosine significantly inhibited 3beta-HSD activity. (2) 0.2 mmol x L(-1) L-tyrosine exerted different effects on 3beta-HSD activity at different concentrations of pregnenolone (Ph). It increased 3beta-HSD activity at 0.1 micromol x L(-1) and 1 micromol x L(-1) of Pn concentration. With further increase in the concentration of Pn to 100 micromol x L(-1), the stimulating effect of L-tyrosine was switched to suppression effect. (3) L-tyrosine and L-tyrosine hydrazide both inhibited 3beta-HSD activity induced by hCG.

CONCLUSIONL-tyrosine affects 3beta-HSD activity of rat luteal cells in vitro. L-tyrosine and tyrosine hydrazide inhibits hCG induced 3beta-HSD activity.

3-Hydroxysteroid Dehydrogenases ; metabolism ; Animals ; Cells, Cultured ; Female ; Luteal Cells ; drug effects ; enzymology ; Rats ; Rats, Wistar ; Tyrosine ; pharmacology

To examine the electrophysiological properties of luteal cells and the relationship between membrane potential and luteal steroidogenic capacity, the membrane potential of luteal cells and the luteal steroidogenesis were measured under different ionic conditions following treatment with various drugs and gonadotropins. The membrane potential of luteal cells did not vary throughout the estrous cycle and was -55 +/- 1 mV. The membrane potential was highly dependent upon the external K+ concentration and was depolarized by the deprivation of external Ca2+, however) there seemed to be a lower K+ permeability in luteal membranes as the presence of 10-9 M valinomycin, a K+ ionophore Caused hyperpolarization from -55 to -91 mV. Luteal progestin production was increased in a high K+ solution but not m a Ca2+-free solution indicating that Ca2+ may be essential for steroid synthesis and/or secretion by luteal cells. Gonadotropins and ouabain induced a depolarization of the membrane potential and stimulated luteal steroidogenesis; however; prostaglandin F2alpha stimulated only steroidogenesis without any changes in membrane potential. These results suggest that the relationship between steroidogenesis and the changes in membrane potential by drugs and gonadotropins is still obscure and remains to be eluridated. The relationship between membrane potential and steroidogenesis in the luteal cell may be dependent upon the availability of intracelluar Ca2+.
Animal ; Corpus Luteum/*metabolism ; Estrus/metabolism ; Female ; Ions ; Luteal Cells/*metabolism ; Membrane Potentials ; Rats ; Rats, Inbred Strains ; Steroids/*biosynthesis ; Support, Non-U.S. Gov't

The present study aimed to investigate the role of platelet-activating factor (PAF) in progesterone synthesis and vascular endothelial growth factor (VEGF) expression in rat luteal cells. Immature (25-28 days old) female Sprague-Dawley rats were injected subcutaneously with 50 IU pregnant mare serum gonadotrophin (PMSG), and 25 IU human chorionic gonadotrophin (hCG) 48 h later, to induce follicular development and luteum formation. On day 6 after hCG administration (the day of hCG administration was the first day), the rats were killed by guillotine and the ovarian luteal cells were collected. After incubation for 24 h, luteal cells were incubated without or with different doses (0.1 μg/mL, 1 μg/mL, 10 μg/mL) of PAF at 37 °C (5% CO(2)) for 24 h, and then progesterone concentration was evaluated by radioimmunoassay (RIA); apoptotic rate and VEGF mRNA expression in luteal cells were assessed by flow cytometry and RT-PCR, respectively. The results showed that PAF promoted progesterone production, with a maximal effect at 1 μg/mL (P<0.05); PAF increased apoptotic rate but not in a dose-dependent manner, and 10 μg/mL PAF enhanced apoptotic rate significantly (P<0.05); furthermore, PAF stimulated VEGF mRNA expression in luteal cells, especially at 1 μg/mL (P<0.01). It is suggested that PAF regulates progesterone synthesis and VEGF mRNA expression in luteal cells to mediate corpus luteum formation in rat ovary.
Animals ; Chorionic Gonadotropin ; pharmacology ; Corpus Luteum ; drug effects ; Female ; Luteal Cells ; drug effects ; metabolism ; Platelet Activating Factor ; pharmacology ; Pregnancy ; Progesterone ; biosynthesis ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A ; metabolism