Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources
PubMed1987

Prostaglandins, chorioamnionitis and preterm labour.

The production of prostaglandin E (PGE) and leukotriene B4 (LTB4) by amnion was measured in vitro in 12 women delivered after spontaneous preterm labour and in 15 women delivered after spontaneous labour at term. The placenta and fetal membranes were examined histologically in all cases. PGE output (fmol/mg dry weight/2 h) in the amnions from uncomplicated preterm deliveries was low (median 486, range 232-3203, n = 7) compared with the values obtained after spontaneous labour at term (5529, 1722-14,226, n = 15). In amnions from preterm deliveries complicated by acute chorioamnionitis or round cell infiltration there was massive release of PGE (15,262, 10,905-27,640, n = 5) which was accompanied by an increase in LTB4 production. Inflammatory infiltration of the fetal membranes results in a huge increase in PG production which could cause preterm labour.

Amnion↗
PubMedDate not supplied

Expression of Fc gamma binding sites on human extraplacental membranes.

Binding sites for the Fc portion of immunoglobulin G (IgG) molecules (Fc gamma BS) were identified on amnionic epithelial cells and chorionic trophoblast cells in human extraplacental membranes using direct immunofluorescence with labeled human IgG. The binding sites are similar to FC gamma BS on placental trophoblast in their specificity and high degree of relative binding affinity for IgG monomers. Neither immunoglobulin A (IgA) nor IgM bound to a significant degree to the membranes. Binding was completely inhibited with unlabeled IgG but not F(ab')2 fragments of IgG. Studies on isolated amnion cells demonstrated that the binding sites are expressed on the cell membrane. At the level of sensitivity of the immunohistologic methods used, aggregated IgG or antigen-antibody complexes failed to bind amnionic epithelial cells or chorionic trophoblasts. This is in contrast to Fc gamma BS on macrophages which, being present in the same tissue, failed to exhibit significant binding of deaggregated IgG but bound complexes avidly.

Amnion↗
PubMed1994

Expression of TNF-alpha and TNFR p55 in cultured amniochorion.

PROBLEM: Preterm labor and PROM are major complications of pregnancy. We have reported the possible role of amniochorionic membrane as it relates to the production of cytokines and the early onset of labor. Amniochorion is capable of responding to an infectious process with the production of IL-6 and IL-1 beta. Here we examine the expression of TNF-alpha and TNFR in amniochorion. METHOD: Amniochorionic membranes were collected and maintained in an organ explant system. Samples were frozen and/or fixed for RT-PCR, in situ hybridization, and immunocytochemistry. RESULTS: RT-PCR demonstrated mRNA for TNF-alpha and in situ hybridization localized mRNA in chorion and amnion. Immunocytochemistry demonstrated TNF-alpha peptide in amnion but not in chorion. Immunocytochemical localization of TNFR indicates presence of that peptide in both amnion and chorion. CONCLUSIONS: We conclude that the fetal membranes are sources of TNF-alpha and TNFR, supporting our previous work indicating that fetal membranes are active participants in the response to intraamniotic infection.

Amnion↗
PubMed1966

Amniotic contraction and embryonic motility in the chick embryo.

During part of the incubation period of chick embryos the amnion shows spontaneous contractions. Removal of the amnion on days 9, 10, and 11 has no effect on the amount of, or the cyclic aspects of, motility exhibited by the embryo. These observations question the importance of the amnion and yolk-sac as stimulative factors in the initiation and maintenance of cyclic embryonic motility at the ages studied.

Amnion↗
PubMed1987

The hyaluronidase associated with Treponema pallidum facilitates treponemal dissemination.

Treponema pallidum contains hyaluronidase (Hase) associated with its surface. Experiments were performed to determine the functional role of this enzyme in syphilitic infection. The effects of incubating organisms with rabbit anti-bovine Hase or normal or immune sera were compared. Preincubation of treponemes with anti-Hase resulted in inhibition of treponemal degradation of hyaluronic acid, indicating that these antisera did in fact retard enzyme activity. Anti-Hase did not immobilize or neutralize T. pallidum. In addition, rabbits were immunized with bovine Hase and then challenged intradermally with organisms; subsequent lesion development was not affected. Anti-Hase did not block treponemal attachment to cultured testicular fibroblasts but did inhibit attachment to isolated capillaries. Rabbit amnions were used as an in vitro model for dissemination of T. pallidum. Anti-Hase retarded the penetration of organisms through the amnions. This inhibitory effect was dependent on the presence of amniotic hyaluronic acid. When this glycosaminoglycan was selectively removed, the anti-Hase lost its ability to inhibit treponemal penetration. When exogenous hyaluronic acid was added back to treated amnions, the inhibitory effect of anti-Hase was restored. Evans blue experiments were used to characterize treponeme-induced vascular leakage following intradermal inoculation of T. pallidum. Prior treatment of organisms with anti-Hase reduced dermal leakage of the dye, indicating the involvement of the treponemal Hase in causing vessel leakage. Finally, rabbit testicular infections were used as an in vivo model for dissemination; one testis was infected, and after 10 to 13 days, treponemes in the opposite testis were quantitated. The anti-Hase restricted dissemination of organisms. These findings point to the functional role of the treponemal Hase in facilitating disseminated syphilis.

Amnion↗
PubMed1998

Immunolocalisation of interleukin-4 and interleukin-4 receptor in placenta and fetal membranes in association with pre-term labour and pre-eclampsia.

The aim of this study was to characterise the localisation and staining intensity of immunoreactive (ir) interleukin-4 (IL-4) and IL-4 receptor (IL-4R) in human placenta and fetal membranes in association with pre-term and term labour, and pre-eclampsia. The data obtained in this study establish the presence of irIL-4 and IL-4R in human placenta and fetal membranes obtained from women at 25-41 completed weeks of gestation. IL-4 and IL-4R immunohistochemical staining was principally localised in villous and chorionic trophoblast, and to amnion epithelial cells. The intensity of IL-4 and IL-4R immunohistochemical staining was not significantly affected by labour status at term or pre-term (p > 0. 05), with the exception of IL-4R in the amnion (p < 0.05). In term amnion, IL-4R was only detectable following labour onset. When data were stratified with respect to the presence or absence of pre-eclampsia, no statistical difference in immunohistochemical localisation or staining intensity for either IL-4 or IL-4R could be identified for any of the tissues studied. Co-localisation of IL-4 and IL-4R within gestational tissues may indicate auto- and/or paracrine mechanisms of action for this cytokine. Tissue-specific, labour-associated induction of IL-4R may contribute to the regulation of biological effects of IL-4 within the uteroplacental unit.

Amnion↗
PubMed1989

Reduction of hydroxyproline content in the vessels of the human umbilical cord in premature rupture.

The hydroxyproline content of the amnion and the umbilical vessels obtained from cases in which the fetal membranes were instrumentally or prematurely ruptured was assayed. Hydroxyproline concentration (in micrograms/mg) in the latter group was 23.76, 16.79 and 17.86 in the amnion, artery and vein, whereas in the former the corresponding values were 42.20, 26.61 and 32.48. These results show that, in addition to a decrease in the amnion, hydroxyproline is lowered also in the umbilical vessels, suggesting that the reduction in the collagen in the fetal membranes is probably a particular manifestation of a general metabolic deficiency.

Amnion↗
PubMed1985

Despite a massive increase in cortisol secretion in women during parturition, there is an equally massive increase in prostaglandin synthesis. A paradox?

In this investigation, we sought to resolve the apparent paradox that is posed by the fact that there is a simultaneous increase in the production of prostaglandin and cortisol in women during labor. A paradox obtains, since in most tissues, cortisol acts to inhibit prostaglandin formation. Using previously characterized model systems for the in vitro study of arachidonic acid metabolism in amnion, decidua, and myometrium, we found that prostaglandin production by amnion and endometrial stromal cells in monolayer culture was not decreased by glucocorticosteroid treatment. On the other hand, prostaglandin production by myometrial smooth muscle cells in culture was inhibited by greater than 90% in response to dexamethasone (10(-7) M) treatment. Importantly, the major prostaglandin produced by myometrium, as well as myometrial smooth muscle cells in culture, is prostacyclin, a prostaglandin that acts to cause uterine quiescence. We suggest that the immunity of amnion and decidua to the action of glucocorticosteroids may allow for the accelerated production of prostaglandins E2 and F2 alpha, which act to cause myometrial contractions; simultaneously, glucocorticosteroid produced in large quantities in women in labor may lead to decreased production of prostacyclin by myometrium, thereby reducing uterine quiescence. In this coordinated manner, the uterine contractions that culminate in delivery of the fetus may proceed uninterrupted in the face of increased cortisol production.

Amnion↗
PubMed2005

The progesterone receptor in human term amniochorion and placenta is isoform C.

The mechanism that initiates human parturition has been proposed to be functional progesterone withdrawal whereby the 116-kDa B isoform of the progesterone receptor (PR-B) switches in favor of the 94-kDa A isoform (PR-A) in reproductive tissues. Recently other PR isoforms, PR-S, PR-C, and PR-M generated from the same gene have been identified and partially characterized. Using immunohistochemical, Western blotting, and RT-PCR techniques, evidence is provided that the major PR isoform present in human term fetal membranes (amnion and chorion) and syncytiotrophoblast of the placenta is neither of the classical nuclear PR-B or PR-A isoforms but is the N terminally truncated 60-kDa PR-C isoform. Evidence is also provided that the PR-C isoform resides in the cytoplasm of the expressing cell types. Data are also presented to show that PR-B, PR-A, and PR-S isoforms are essentially absent from the amnion and chorion, whereas PR isoforms A, B, C, and S are all present in the decidua, with PR-A being the major isoform. The syncytiotrophoblast of the placenta contains the cytoplasmic PR-C isoform but not PR-A, PR-B, or PR-S. The major PR isoform in the amnion, chorion, and placenta is PR-C, suggesting that the cytoplasmic PR-C isoform has a specific role in extraembryonic tissues and may be involved in the regulation of human parturition.

Amnion↗
PubMed1988

Vasopressin metabolism in the amniotic sac of the fetal guinea pig.

A route for fetal 8-arginine vasopressin (AVP) clearance has not yet been established. The results of this study indicate that in the fetal guinea pig, the amniotic sac is a site for AVP metabolism. When fetal plasma, urine, and amniotic fluid were fractionated on HPLC, AVP was identified only in fetal plasma and urine. In addition, when AVP and inulin were injected into the amniotic sac in vivo during the last week of gestation, the AVP to inulin ratio decreased (P less than 0.05) over a 2-h period, indicating a swallowing-independent disappearance of AVP. Furthermore, when tritiated AVP was similarly injected, the radioactivity to inulin ratio remained constant, suggesting that AVP was not diffusing out of the amniotic sac. Two hours after the injection into the amniotic sac, amniotic fluid was collected and fractionated by HPLC, and only 42% of the total radioactivity was intact AVP. The remainder was identified in two other products (M1 and M2). Tritiated AVP incubated with amniotic fluid and amnionic membrane in vitro produced both M1 and M2. Tritiated AVP incubated with amnionic membrane in artificial amniotic solution produced only M1. Tritiated AVP incubated in only amniotic fluid produced M2, with only slight M1 production. Thus, neither metabolite was necessary for the production of the other; M1 was amnionic membrane dependent, and M2 was amniotic fluid dependent. In conclusion, the amniotic sac may play a role in the clearance of AVP from the fetal system.

Amnion↗
PubMed2003

Late gestation increase in 11beta-hydroxysteroid dehydrogenase 1 expression in human fetal membranes: a novel intrauterine source of cortisol.

Late human gestation is associated with an increase in the concentration of cortisol (F) in the fetal circulation and amniotic fluid. It had been assumed that most of the F measured in the amniotic fluid came from the fetal adrenal gland. However, local production of F can also occur in human intrauterine tissues from inactive cortisone under the influence of the enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1. Recent studies have shown that 11beta-HSD 1 activity is up-regulated by prostaglandins (PG) E2 and F2alpha, hormones that are produced in the fetal membranes (FM) at term. In the present study, we hypothesized that 11beta-HSD 1 expression would increase in FM during pregnancy and at labor, creating the potential for local increase in F production at term. We examined 11beta-HSD 1 expression in placenta and FM obtained during normal pregnancy from nonlaboring women [26-28 wk (n = 3); 29-30 wk (n = 3); 32-33 wk (n = 3); 35-36 wk (n = 3)] and from uncomplicated term pregnancies after elective cesarean section (n = 6). 11beta-HSD 1 expression was also examined in amnion and chorionic tissues in relation to term labor (n = 12). Immunohistochemistry and Western blot analysis were used to examine 11beta-HSD 1 localization and expression. 11beta-HSD 1 activity was also measured in microsomal fractions prepared from whole fetal membranes. At term, immunoreactive 11beta-HSD 1 expression was localized predominantly to the chorion trophoblast cells, attached decidua, and amnion epithelial cells. 11beta-HSD 1 expression in FM increased with gestational age and reflected increased enzyme reductase activity. No change in 11beta-HSD 1 expression was found in placental tissue from the same patients. There was a significant increase in 11beta-HSD 1 expression in amnion but not in chorion with the onset of labor. We suggest that increases in 11beta-HSD 1 expression/activity by intrauterine membranes during late gestation may result in increased potential for a local increase in F production and that FM should be considered as an extraadrenal source of F during late gestation. This local F production may be involved in different pathways contributing to the regulation of parturition.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2004

Regulation of phospholipase isozymes by nuclear factor-kappaB in human gestational tissues in vitro.

Phospholipid-derived mediators are implicated in the initiation and progression of human labor and delivery, particularly in relation to infection-induced preterm labor. We previously demonstrated that, in human intrauterine tissues, lipopolysaccharide (LPS)-stimulated nuclear factor-kappaB (NF-kappaB) DNA binding activity, and subsequent cytokine release can be suppressed by sulfasalazine (SASP) concentrations greater than 5 mM. The aim of this study was to elucidate the effect the SASP on secretory type II phospholipase A(2) (PLA(2)), cytosolic PLA(2) (cPLA(2)), cyclooxygenase (COX) isozymes, and subsequent prostaglandin F(2alpha) (PGF(2alpha)) production in human gestational tissues. Human placenta, amnion, and choriodecidua (n = 4-9 separate placentas) were incubated in the presence of SASP (0.1, 1, 5, and/or 10 mM) under either basal or LPS (10 microg/ml) conditions. After 6 h incubation, the tissues were collected and assayed for type II PLA(2) by ELISA and cPLA(2), COX-1, and COX-2 content by Western blotting. The incubation medium was collected and assayed for type II PLA(2) and 13,14-dihydro-15-keto PGF(2alpha) release by ELISA and PGF(2alpha) by RIA. Treatment of placenta, amnion, and choriodecidua with SASP concentrations greater than 5 mM significantly inhibited basal and/or LPS-stimulated type II PLA(2) content and release, 13,14-dihydro-15-keto PGF(2alpha) release, and cPLA(2) protein content (ANOVA, P < 0.05); however, no effect of SASP was observed on basal or LPS-stimulated COX-1 or COX-2 protein. Although no effect of SASP was observed on basal and LPS-stimulated PGF(2alpha) release from placenta and amnion, it significantly increased both basal and LPS-stimulated PGF(2alpha) release from choriodecidua. In addition, SASP concentrations of 5 mM or greater significantly suppressed NF-kappaB DNA binding activity. These data are consistent with the hypothesis that NF-kappaB regulates the expression and release of phospholipase isozymes.

Amnion↗
PubMed1994

Immunohistochemical localization, messenger ribonucleic acid abundance, and activity of 15-hydroxyprostaglandin dehydrogenase in placenta and fetal membranes during term and preterm labor.

Type 1 15-hydroxyprostaglandin dehydrogenase (PGDH) is the main enzyme responsible for the metabolism of prostaglandin E2 (PGE2) and PGF2 alpha. To examine the possibility that a deficiency of PGDH might contribute to preterm labor, we measured localization of immunoreactive (IR-) PGDH, PGDH mRNA, and PGDH enzyme activity in chorio-decidua, placenta, and amnion in patients after term elective cesarean section (n = 9), after spontaneous vaginal term delivery (n = 10), and at idiopathic preterm labor (PTL) in the absence of infection (< 36 weeks gestation; n = 11). Localization of IR-PGDH was determined in additional specimens of membranes after PTL with infection (n = 13) and without (n = 37). IR-PGDH was localized in syncytiotrophoblast and intermediate trophoblasts in placenta and in the trophoblast layer of extraplacental chorion, but was absent from amnion in all patient groups. In chorion, the number of IR-positive trophoblasts was significantly reduced in the idiopathic PTL group compared to those in the other groups. The relative abundance of PGDH mRNA in the chorio-decidua, but not the placenta, from spontaneous labor and PTL was significantly less than that after cesarean section. PGDH mRNA in chorio-decidua from preterm patients correlated with PGDH enzyme activity. Undetectable or low IR-PGDH in chorionic trophoblasts was also associated with low enzyme activity. These results suggest that there exists a subset of patients that present in PTL because of reduced PGDH expression in chorionic trophoblasts. We suggest that this relative deficiency would allow PGs synthesized in the amnion or chorion to escape metabolism in the chorion and thereby contribute to the stimulus to idiopathic PTL.

Amnion↗
PubMed1997

Epidermal growth factor receptors in uteroplacental tissues in term pregnancy before and after the onset of labor.

Using saturation binding assays and Scatchard analyses, we determined the concentrations and binding affinities of epidermal growth factor (EGF) receptors in human myometrium (n = 13) and decidua (n = 10) before and during labor and in placenta (n = 15), chorion (n = 17), and amnion (n = 17) before labor, during labor, and after vaginal delivery. Each tissue was individually assayed. In myometrium and chorion, EGF receptors increased significantly from 5.6 +/- 0.8 and 13.5 +/- 1.7 fmol/mg protein (mean +/- SEM) before labor to 11.1 +/- 2.8 and 26.7 +/- 3.0 fmol/mg protein, respectively, after the onset of labor (P < 0.05). In amnion, EGF receptors increased from 12.8 +/- 2.7 fmol/mg protein before labor to 33.0 +/- 2.3 fmol/mg protein during labor, but decreased significantly (5.9 +/- 1.2 fmol/mg protein) with vaginal delivery (P < 0.05). Decidual and placental concentrations of EGF receptors did not change significantly with labor. The binding affinity of EGF receptors in all tissues studied did not change significantly with labor, as reflected by their respective association and dissociation constants. Up-regulation of EGF receptors in myometrium, chorion, and amnion with spontaneous labor may enhance stimulation of prostanoid production and stimulate uterine activity.

Amnion↗
PubMed1997

Differential expression of 11 beta-hydroxysteroid dehydrogenase types 1 and 2 in human placenta and fetal membranes.

Two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) are present in mammals. 11 beta HSD1 interconverts biologically active cortisol and inactive cortisone, whereas 11 beta HSD2 only converts cortisol to cortisone. Placental 11 beta HSD has been proposed to protect the fetus from high level of maternal glucocorticoids. Although bidirectional activity of 11 beta HSD has been demonstrated in homogenized human placental tissues, the tissue and cellular distribution of 11 beta HSD1 has not been resolved. In this study, the cellular localization of 11 beta HSD1 protein and levels of its messenger ribonucleic acid (mRNA) in human placenta and fetal membranes were determined by immunohistochemistry and Northern blot analysis, respectively. We found that 11 beta HSD1 immunoreactivity was present in the placental extravillous intermediate trophoblasts, chorion trophoblasts, amnion epithelial cells, and stromal cells of the decidua vera. Positive staining was also observed in the endothelium of the blood vessels in both placental villous tissue and umbilical cord. However, in contrast to previous reports of immunoreactive 11 beta HSD2 localization, 11 beta HSD1 immunoreactivity was undetectable in placental syncytiotrophoblast. Using a human 11 beta HSD1 complementary DNA as probe, a 1.5-kilobase mRNA transcript was detected in the chorion, amnion, and placental tissue, with the greatest amount in the chorion. In contrast, the 1.9-kilobase mRNA of 11 beta HSD2 was observed only in the placenta, not in the chorion and amnion. The process of labor had no significant effect on levels of 11 beta HSD1 or 11 beta HSD2 mRNA in the chorion or placenta. We conclude that there is a striking difference in the tissue localization of 11 beta HSD1 and 11 beta HSD2 expression in the late gestation human placenta and fetal membranes, which may discretely determine the accessibility of bioactive glucocorticoid to specific cell types.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2001

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm.

The murine Foxf1 gene encodes a forkhead transcription factor expressed in extra-embryonic and lateral plate mesoderm and later in splanchnic mesenchyme surrounding the gut and its derivatives. We have disrupted Foxf1 and show that mutant embryos die at midgestation due to defects in mesodermal differentiation and cell adhesion. The embryos do not turn and become deformed by the constraints of a small, inflexible amnion. Extra-embryonic structures exhibit a number of differentiation defects: no vasculogenesis occurs in yolk sac or allantois; chorioallantoic fusion fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers. Separation of the bulk of yolk sac mesoderm from the endodermal layer and adherence between mesoderm of yolk sac and amnion, indicate altered cell adhesion properties and enhanced intramesodermal cohesion. A possible cause of this is misexpression of the cell-adhesion protein VCAM1 in Foxf1-deficient extra-embryonic mesoderm, which leads to co-expression of VCAM with its receptor, alpha(4)-integrin. The expression level of Bmp4 is decreased in the posterior part of the embryo proper. Consistent with this, mesodermal proliferation in the primitive streak is reduced and somite formation is retarded. Expression of Foxf1 and the homeobox gene Irx3 defines the splanchnic and somatic mesodermal layers, respectively. In Foxf1-deficient embryos incomplete separation of splanchnic and somatic mesoderm is accompanied by misexpression of Irx3 in the splanchnopleure, which implicates Foxf1 as a repressor of Irx3 and as a factor involved in coelom formation.

Allantois↗
PubMed2000

[Apoptotic cell death induced by actinomycin D arisen at different levels and cell cycle stages according to human cultured cell species].

Nine kinds of human cultured cells, including fetus cells (smooth chorion trophoblast cells, amnion epithelial cells and HE-21), adult non-carcinoma cells (HCF), and carcinoma cells (KATO-III, COLO 201, Lu-134-AH, SK-OV-3 and SKG-3a) were stimulated with Actinomycin (Act.) D for 24 h. Apoptosis induction was investigated by agarose gel electrophoresis for DNA fragmentation analysis and by flow cytometric analysis of stained cells using in situ terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP nick-end labeling TUNEL) staining techniques for the quantification of apoptosis, and simultaneously using propidium iodide for the gain of some information about cell cycle. By agarose gel electrophoresis, DNA fragmentation of these cells except amnion epithelial and SKG-3a cells was detected, depending on concentration of Act. D. Using flow cytometric analysis, these cells were separated into four groups according to the information about cell cycle. Group 1 included amnion epithelial and SKG-3a cells, which were TUNEL negative. In group 2, all cell populations at G0/G1 and G2/M phases of HCC, KATO-III and SK-OV-3 were TUNEL staining positive. A portion of each G0/G1 or G2/M phase cell of Lu-134-AH and COLO 201 in group 3 was TUNEL stain positive. In group 4, G2/M phase cells of smooth chorion trophoblast cells and HE-21 were mostly stained and a small population of G0/G1 phase cells were also TUNEL stain positive. These results show that the stages of the cell cycle at which apoptosis was arisen by Act. D stimulation were significantly different depending on the cells types.

Amnion↗
PubMed2003

Expression of membrane prostaglandin E synthase in human placenta and fetal membranes and effect of labor.

Initiation and maintenance of labor in humans is associated with an increase in prostaglandin synthesis by intrauterine tissues. The objective of the present study was to characterize the distribution of membrane-bound PGES (mPGES) protein and mPGES mRNA in human placenta, fetal membranes, and decidua at term and to determine whether any changes occurred with labor. Immunoreactive mPGES was found to be highly concentrated in amnion epithelial cells and the chorion laeve trophoblasts, with lower levels in the mesenchymal layers. The enzyme was at very low levels or undetectable in the decidual tissue. Much lower levels of mPGES protein and mRNA were found in placenta than in fetal membranes. mPGES was associated with the syncytiotrophoblast and in cells surrounding blood vessels. The expression of mPGES mRNA did not change with labor in full membranes or placenta, but Western analysis showed an increase in mPGES protein in chorion laeve and a decrease in mPGES protein in placenta during labor, with no change in the amnion. The differences in expression found among placenta, chorion, and amnion before and after labor would indicate that this enzyme is differentially regulated in these tissues at this time.

Adult↗