| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Regular Article |
a Canadian Institutes for Health Research Groups in Fetal and Neonatal Health and Development, Departments of Physiology and Obstetrics and Gynecology, University of Toronto, Toronto, Ontario, Canada M5S 1A8
b Departments of Obstetrics and Gynecology and Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8L6
Recent evidence suggests that ovine placental output of prostaglandin (PG) E2 rises through late gestation partly because of a direct effect of cortisol on PGH2 synthase 2 (PGHS-2) expression and activity within trophoblast tissue. Synthesis of PGE2 is also dependent, however, on PGE2 synthase (PGES), which converts PGH2 to PGE2. We hypothesized that PGES is expressed in the ovine placenta, and that, similar to PGHS-2, expression increases through gestation and is regulated positively by cortisol. Placental tissues from pregnant ewes in mid and late gestation, at term, and during early and active labor were analyzed to determine the gestational profile of PGES. The regulation of PGES expression was assessed in placental tissues from pregnant ewes in which intrafetal cortisol infusion was administered in late gestation, in the presence or absence of an aromatase inhibitor, to block the cortisol-stimulated rise in estradiol. Expression of PGES was analyzed by in situ hybridization, Western blot analysis, and immunohistochemistry. In the placentome, PGES localized to fetal trophoblast cells and endothelial cells in maternal blood vessels, consistent with its contribution to the rise in placental PGE2 output toward the onset of labor and with a role of PGE2 in the local regulation of uteroplacental blood flow, respectively. Expression of PGES mRNA and protein increased with gestation. However, there was no significant further change with labor or during cortisol infusion in the presence or absence of a rise in fetal plasma estradiol, in contrast to reported changes in PGHS-2. These results suggest that PGES is not coregulated with PGHS-2 in the sheep placenta at term. The progressive increase in PGES, however, likely contributes to the rise in circulating PGE2 in the fetus in late pregnancy.
1 We gratefully acknowledge the support of the Canadian Institutes for Health Research (CIHR, operating grant MOP 14097) and the CIHR Group in Development and Fetal Health.
2 Correspondence: J.R.G. Challis, Department of Physiology, Medical Sciences Building, University of Toronto, 1 King's College Circle, Toronto, ON, Canada M5S 1A8. FAX: 416 978 4940; j.challis{at}utoronto.ca
This article has been cited by other articles:
|
|
 |
|
  Q. Zhang, V. Collins, K. Chakrabarty, R. F. Wolf, N. Unno, D. Howe, J. C. Rose, and W. X. Wu Regulation of Membrane-Associated Prostaglandin E2 Synthase 1 in Pregnant Sheep Intrauterine Tissues by Glucocorticoid and Estradiol Endocrinology, August 1, 2006; 147(8): 3719 - 3726. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Sun, R. Ma, X. Cui, B. Campos, R. Webster, D. Brockman, and L. Myatt Glucocorticoids Induce Cytosolic Phospholipase A2 and Prostaglandin H Synthase Type 2 But Not Microsomal Prostaglandin E Synthase (PGES) and Cytosolic PGES Expression in Cultured Primary Human Amnion Cells J. Clin. Endocrinol. Metab., November 1, 2003; 88(11): 5564 - 5571. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Giannoulias, N. Alfaidy, A. C. Holloway, W. Gibb, M. Sun, S. J. Lye, and J. R. G. Challis Expression of Prostaglandin I2 Synthase, but Not Prostaglandin E Synthase, Changes in Myometrium of Women at Term Pregnancy J. Clin. Endocrinol. Metab., November 1, 2002; 87(11): 5274 - 5282. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
