Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen

Riley, Simon C.; Leask, Rosemary; Selkirk, JV; Rw, Kelly; An, Bo; Howe, DC

doi:10.1530/jrf.0.1190329

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2000

DOI: 10.1530/jrf.0.1190329

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Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen

Simon C. Riley

Rosemary Leask²,

JV Selkirk³

et al.

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Cited by 3 publications

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“…METHODS: To test the hypotheses, we infused singleton, chronically catheterized fetal sheep beginning at day 125 ofgestation (tenr 147 to 150 days) with (1) cortisol (0.45 mg/mL; n = 5); (2) cortisol and 4-hydroxyandrostenedlione, a P450aromnaise inhibitor (4-OHA: 1.44 mg/h; ii = 5); (3) saline (n = 5); or (4) saline and 4-OHA (n = 5). PGHS-II, ERlk, ERf3, and GRaiwere localized using immunohistochemistry.…”

mentioning

confidence: 99%

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

Whittle

Holloway

Lye

et al. 2006

Journal of the Society for Gynecologic Investigation

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We concluded that the differential effects of cortisol and estradiol on intrauterine PGHS-II expression and PG production may be due to the tissue-specific expression of the GR and ER within the intrauterine tissues. Glucocorticoid effects on trophoblast PG production may be mediated in a positive feed-forward manner. We further suggest that either cortisol or a cortisol-stimulated intermediate, like PGE2, increased P450(C17) expression, leading to a rise in placental estradiol synthesis and triggering maternal intrauterine tissue PG production.

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mentioning

confidence: 99%

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

Whittle

Holloway

Lye

et al. 2006

Journal of the Society for Gynecologic Investigation

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Prostaglandin Production at the Onset of Ovine Parturition Is Regulated by Both Estrogen-Independent and Estrogen-Dependent Pathways¹

Whittle

Holloway²,

Lye³

et al. 2000

Endocrinology

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A current hypothesis of ovine parturition proposes that fetal adrenal cortisol induces placental E2 production, which, in turn, triggers intrauterine PG production. However, recent evidence suggests that cortisol may directly increase PG production in trophoblast-derived tissues. To separate cortisol-dependent and estrogen-dependent PG production in sheep intrauterine tissues, we infused singleton, chronically catheterized fetuses beginning on day 125 of gestation (term, 147-150 days) with 1) cortisol (1.35 mg/h; n = 5); 2) cortisol and 4-hydroxyandrostendione, a P450aromatase inhibitor (4-OHA: 1.44 mg/h; n = 5); 3) saline (n = 5); or 4) saline and 4-OHA (n = 5). Fetal and maternal arterial blood samples were collected at 12-h intervals starting 24 h before infusion and continuing during treatment for 80 h or until active labor. Uterine contractility was measured by electromyogram recording of myometrial activity. Plasma E2, progesterone (P4), PGE2, and 13,14-dihydro- 15-keto-PGF2alpha were quantified by RIA. PGHS-II messenger RNA (mRNA) and protein expression were determined by in situ hybridization and Western blot analysis, respectively. Data were analyzed by ANOVA (P < or = 0.05). Labor-type uterine contractions were present after 68 h of cortisol infusion and had increased significantly by 80 h. Labor-type uterine contractions were induced after 68 h of cortisol plus 4-OHA infusion, but the contraction frequency remained less than that in the cortisol-treated animals. Fetal cortisol infusion increased fetal and maternal plasma E2 concentrations and decreased the maternal plasma P4 concentration significantly; concurrent 4-OHA infusion attenuated the increase in fetal and maternal plasma E2, but not the decrease in maternal plasma P4. The fetal plasma PGE2 concentration increased after both cortisol and cortisol plus 4-OHA infusion. The maternal plasma 13,14-dihydro-15-keto-PGF2alpha concentration rose after fetal cortisol infusion, but not after cortisol plus 4-OHA infusion. Placental trophoblast PGHS-II mRNA and protein expression were increased significantly after both cortisol and cortisol plus 4-OHA infusion. Endometrial PGHS-II mRNA and protein expression increased after cortisol infusion, but not after cortisol plus 4-OHA infusion. Plasma steroid and PG concentrations, uterine activity pattern, and intrauterine PGHS-II expression were not altered in either control group. We conclude that these data suggest distinct pathways of intrauterine PG synthesis: a cortisol-dependent/E2-independent mechanism within trophoblast tissue leading to elevations in fetal plasma PGE2, and an E2-dependent mechanism within maternal endometrium that leads to increased maternal plasma PGF2alpha and appears necessary for uterine activity and parturition.

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Differential Changes in 15-Hydroxyprostaglandin Dehydrogenase and Prostaglandin H Synthase (Types I and II) in Human Pregnant Myometrium

Giannoulias

Patel

Holloway

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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Prostaglandins (PGs) play a key role in the onset of labor in many species and regulate uterine contractility and cervical dilatation. Therefore, the regulation of prostaglandin output by PG synthesizing (PGHS-I and PGHS-II) and metabolizing (PGDH) enzymes in the human myometrium may determine uterine activity patterns in human labor both at preterm and at term. We hypothesized that expression of PGHS isozymes and PGDH in myometrium from women at preterm and term labor would change to favor increased uterotonin (PG) production. Myometrial samples were obtained from the lower uterine segment during cesarean section deliveries from women presenting in preterm, no labor; preterm, labor; term, no labor; term, labor. Immunoreactive (ir-) PGHS and PGDH protein was localized using immunohistochemistry, and changes in protein levels were determined by Western blotting. Ir-PGHS-I and PGHS-II proteins were localized only to myocytes. Ir-PGDH was localized to myocytes in all samples of myometrium examined, but using dual immunofluorescence and immunohistochemistry, ir-PGDH was also detected in cells of the connective tissue. Levels of ir-PGHS-I and PGHS-II protein were not significantly different between no labor and labor tissues, either at preterm or at term. There was no significant effect of gestational age on levels of PGDH, PGHS-I, and PGHS-II protein, but there was a significant decrease in ir-PGDH protein levels in myometrium with labor both at preterm and at term. In addition, there was a decrease in PGDH activity in myometrium from women in labor, both at preterm and at term. Therefore, we conclude that PGDH, PGHS-I, and PGHS-II protein localize within the myocytes of the human pregnant myometrium. A decrease in PGDH protein and activity occurs in association with active labor and may contribute to the amount of bioactive PGs available to act within the human pregnant myometrium at that time.

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Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen

Cited by 3 publications

References 17 publications

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

Prostaglandin Production at the Onset of Ovine Parturition Is Regulated by Both Estrogen-Independent and Estrogen-Dependent Pathways¹

Differential Changes in 15-Hydroxyprostaglandin Dehydrogenase and Prostaglandin H Synthase (Types I and II) in Human Pregnant Myometrium

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Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen

Cited by 3 publications

References 17 publications

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

The Pattern of Glucocorticoid and Estrogen Receptors May Explain Differences in Steroid Dependency of Intrauterine Prostaglandin Production at Parturition in Sheep

Prostaglandin Production at the Onset of Ovine Parturition Is Regulated by Both Estrogen-Independent and Estrogen-Dependent Pathways1

Differential Changes in 15-Hydroxyprostaglandin Dehydrogenase and Prostaglandin H Synthase (Types I and II) in Human Pregnant Myometrium

Contact Info

Product

Resources

About

Prostaglandin Production at the Onset of Ovine Parturition Is Regulated by Both Estrogen-Independent and Estrogen-Dependent Pathways¹