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PubMedDate not supplied

New invasion assay using endothelial cells grown on native human basement membrane.

A new invasion assay is introduced using endothelial cells grown on native human basement membrane (BM). The source of the BM was human amnion. The amnion is a uniform tissue composed of an epithelial layer resting on a continuous basement membrane overlying an avascular collagenous stroma. The epithelium was removed exposing the basement membrane (BM) surface. Human umbilical cord endothelium or bovine capillary endothelium were cultivated on the BM surface. Human squamous carcinoma cells were inoculated onto the BM surface in the presence or absence of the endothelial monolayer. Tumor cells attached readily to both the endothelial monolayer or the BM surface alone. Tumor cells which invaded the basement membrane and underlying collagenous connective tissue were collected on a Millipore filter applied to the opposite side of the amnion. Tumor cells invaded the devitalized amnion connective tissue in the absence of endothelium. The presence of either bovine or human endothelium significantly reduced the rate of tumor cell invasion. This system should be useful for further quantitative studies of the interaction between endothelium and tumor cells with regard to the mechanism of invasion.

Animals↗
PubMed1980

Immunohistochemical location of placental proteins (PP8, 9, 10, 11, 12) in human term placentae.

By using an immunoglobulin enzyme bridge (PAP) technique, the location of two ubiquitous tissue proteins (PP8, PP9) and three placental specific tissue proteins (PP10, PP11, PP12) was investigated in ethanol/acetic acid-fixed paraffin-embedded human term placentae. PP8 was found mainly in both the cytoplasm and the nucleus of trophoblast cells (chorion) and syncytiotrophoblast (villi). PP9 was found in the cytoplasm of trophoblast cells (chorion), the fibrous part of interstitial connective tissues (villi), and the cytoplasm of histiocytes (villi, amnion, and decidua). PP10 was found in the cytoplasm of epithelium (amnion) and in both the cytoplasm and the nucleus of syncytiotrophoblast (villi). PP12 was found in the cytoplasm of histiocytes in decidua, amnion, and chorion and the cytoplasm of syncytiotrophoblast (villi). In addition, stains for PP8, PP10, and PP12 were taken up by the cytoplasm of histiocytes found in amnion, villi, the intervillous space, and decidua, in contrast to PP11, which was found to be specific to the cytoplasm of trophoblast cells (chorion and villi). Possible clinical applications of these findings are discussed.

Cell Nucleus↗
PubMed2006

Detection of HCMV DNA in placenta, amniotic fluid and fetuses of seropositive women by nested PCR.

Human cytomegalovirus (HCMV) is the most common viral cause of intrauterine infection throughout the world. Its distribution patterns in different clinical samples are poorly understood. This study was performed to determine the frequency of CMV DNA positivity in maternal/fetus sera, placentas and amniotic fluid, together with maternal/fetus serology. Clinical specimens were obtained from 92 pregnant women who delivered by cesarean section. 98% of women and their neonates were HCMV IgG positive and 5.4% of these mothers were IgM positive, while no IgM was detected in neonates of IgM positive mothers. Among the IgG positive mothers, IgM was detected in 3.3% of their fetuses. 5.4% and 3.3% of maternal and fetal sera were HCMV DNA positive, respectively. The three neonates who were positive for HCMV DNA in sera were also positive for HCMV IgM and the PCR of their amnions was positive (p < 0.0001). 9.8% of placenta samples and 4.3% of amniotic fluid specimens were positive for HCMV DNA while among these placenta samples, two amnions were PCR positive (p = 0.046). Our results showed that there is not always a correlation between placenta and amnion infections. This may be due to reactivation of HCMV leading to placenta infection, as all affected placentas do not pass infection to fetuses and amniotic fluids. Detection of HCMV DNA in amnion and fetus plasma and the existence of fetus IgM against HCMV can also occur without clinical symptoms.

Amniotic Fluid↗
PubMed1995

Vascular endothelial growth factor gene expression in ovine placenta and fetal membranes.

OBJECTIVE: The purpose of this study was to explore the gene expression of vascular endothelial growth factor (VEGF) in placental cotyledon, chorion, and amnion of the ovine fetus. STUDY DESIGN: Time-dated pregnant sheep with singleton or twin fetuses at a gestational age ranging from 100 to 140 days were used for the study. Placental cotyledonary, chorionic, and amniotic tissues were collected and processed for messenger ribonucleic acid analysis by Northern blotting and reverse transcription-polymerase chain reaction. RESULTS: By use of a phosphorus 32-labeled human VEGF complementary deoxyribonucleic acid probe, a prominent VEGF messenger ribonucleic acid transcript of 3.7 kb was detected in the cotyledon, chorion, and amnion. A minor band of 1.7 kb was also found but only in the cotyledon and chorion. The abundance of messenger ribonucleic acid encoding VEGF was highest (p < 0.001) in the cotyledon and lowest in the amnion. In these tissues polymerase chain reaction-amplified products corresponding to VEGF121, VEGF165, VEGF189, and VEGF206 were identified by ethidium bromide. In addition, a polymerase chain reaction fragment corresponding to VEGF145 was observed. These fragments produced specific hybridization signals with the human VEGF radioactive probe where the intensity of the signal was strongest for VEGF165 and weakest for VEGF189. CONCLUSIONS: VEGF gene expression was detected in the cotyledon, chorion, and amnion of the near-term ovine fetus. These findings suggest that vascular endothelial growth factor may play a role in the induction of angiogenesis and promotion of permeability in the microvessels that perfuse the placental and fetal membranes.

Animals↗
PubMed1993

Type II phospholipase A2 in human gestational tissues: extractable immuno- and enzymatic activity in fetal membranes.

In this study, we have established the presence of immunoreactive (ir) Type II PLA2 in human amnion and choriodecidua obtained from women at term prior to the onset of labour. The content of irType II PLA2 present in 1 M NaCl extracts of choriodecidua and amnion averaged 3.5 +/- 3.1 and 10.6 +/- 5.2 ng/mg tissue protein (n = 3), respectively. PLA2 enzymatic activity present in the same tissues averaged 1.3 +/- 0.2 and 1.9 +/- 0.7 nmol phosphatidylethanolamine (PE) hydrolysed/mg tissue protein per h (n = 3), respectively. To allow intra-patient comparison of the relative distribution in gestational tissues, irType II PLA2 and PLA2 enzymatic activity was also determined in placenta obtained from the same group of women, and averaged 26.0 +/- 7.0 ng/mg tissue protein and 3.5 +/- 1.0 nmol PE hydrolysed/mg protein per h (n = 3), respectively. As has been previously reported for human placenta, the recovery of Type II PLA2 and PLA2 enzymatic activity from amnion and choriodecidua was increased between 16- and 25-fold when tissues were homogenized in high-ionic strength media (i.e., 10% (w/v) ammonium sulphate or 1 M NaCl) compared with that recovered when tissues were homogenized in low-ionic strength media (i.e., 0.32 M sucrose-20 mM Hepes). The data obtained represent the first quantitative estimates of immunoreactive Type II PLA2 in human amnion and choriodecidua, and support the conclusion that previous analyses of the PLA2 enzymatic activity present in gestational tissues have essentially excluded the contribution made by this PLA2 isozyme to net enzymatic activity. We suggest that this isozyme represents a major component of the PLA2 enzymatic activity present in human gestational tissues at term and that it contributes significantly to the phospholipid metabolism and arachidonic acid release which occurs during late pregnancy and at the time of labour.

Extraembryonic Membranes↗
PubMed1977

Gas exchange and acid-base regulation in the blood and extraembryonic fluids of the developing chicken embryo.

Measurements of pH, PCO2, PO2 and total CO2 were recorded simultaneously in samples of chorioallantoic fluid, amnionic fluid and blood of the chorioallantoic artery from chicken embryos on days 8, 10, 12, 14, 16, 17 and 18 of incubation. During the incubation period studied, PCO2 levels similarly increased in the blood and extraembryonic fluids. The pH of the blood and amnionic fluid remained approximately constant while the chorioallantoic fluid became progressively acidic. Increases of amnionic fluid and blood HCO-3 indicated that respiartory compensation processes regulate pH. In addition, the disappearance of chorioallantoic fluid HCO-3 suggested that reabsorptive processes may conserve these ions and contribute them to the amnionic fluid by either a direct transfer through the amnioallantoic membrane or by way of the chorioallantoic vascular system.

Acid-Base Equilibrium↗
PubMed1990

Antiprogestagenic inhibition of uterine prostaglandin inactivation: a permissive mechanism for uterine stimulation.

The use of antiprogestins as abortifacients is more effective when antiprogestin priming is followed by the administration of a small dose of synthetic prostaglandin. This increased myometrial sensitivity towards PG has not been explained and experiments in the guinea-pig where no myometrial activity is observed after 48 h of antiprogestin administration together with measurements of PG metabolites in uterine vein blood have given rise to the suggestion that prostaglandin synthesis is inhibited by antiprogestins. We have treated groups of 50 day pregnant guinea-pigs with 10 mg RU486 or vehicle alone and examined the ability of homogenised uterine tissues (myometrium/decidua, cervix, chorion and amnion) to metabolize PGE when given a large excess of substrate and sufficient cofactors. In addition we have examined the ability of these homogenates to synthesis PG. Antiprogestin treatment in vivo resulted in a 9-fold reduction in metabolic activity in chorion (P less than 0.02) and a 4-fold reduction in myometrium/decidua (P less than 0.02). Reduction in activity seen in amnion and cervix was not significant. The maximum metabolism was seen in the chorion and minimal metabolism in the amnion. Maximum PG production was seen in the amnion and minimum in the chorion. These results show that the effect of antiprogestin in reducing prostaglandin catabolism would reduce the threshold above which PG production would cause contractions which would in turn stimulate PG production. Thus an explanation is provided of how low doses of exogenous PGs or transient synthesis of endogenous PG within an antiprogestin treated uterus can led to a self sustaining cycle of stimulation which will lead to abortion.

Amino Acid Sequence↗
PubMed2004

Maternal origin of inflammatory leukocytes in preterm fetal membranes, shown by fluorescence in situ hybridisation.

The aim of this study was to determine the maternal or fetal origin of inflammatory leukocytes in fetal membranes from cases of chorioamnionitis. Fetal membranes were collected from male preterm infants and chorioamnionitis was diagnosed histologically. Fluorescence in situ hybridisation for X and Y chromosomes was used to determine the gender of infiltrating leukocytes in the chorion and amnion. Leukocytes, trophoblast and mesenchymal cells were identified using immunohistochemistry for CD45, cytokeratin-7 and vimentin, respectively. Leukocytes present in the chorion and amnion were labelled XX, indicating maternal origin, and these cells were immunoreactive for the leukocyte marker CD45 but not for vimentin or cytokeratin-7. All other cells in the chorion and amnion were labelled XY and of fetal origin. The results indicated that maternal leukocytes invade the amnion and chorion in chorioamnionitis and we suggest that this is part of the maternal inflammatory response to intrauterine infection.

Adult↗
PubMed1987

Steroid synthetic and prostaglandin metabolizing activity is present in different cell populations from human fetal membranes and decidua.

We examined whether different cell subpopulations from human fetal membranes and decidua produce steroids (estrone and progesterone) and metabolize prostaglandins (prostaglandin F2 alpha to 13, 14-dihydro-15-keto-prostaglandin F2 alpha and if these changed with labor. Amnion, chorion, and decidua were obtained at elective cesarean section at term or at spontaneous labor. Cells were dispersed with collagenase and separated by density on discontinuous Percoll gradients. At cesarean section there was a major broad band of cells from amnion and chorion. This band contained most of the estrone sulfatase (estrone sulfate to estrone) activity. The 3 beta-hydroxysteroid dehydrogenase (pregnenolone to progesterone conversion) and prostaglandin F2 alpha metabolizing activities were present in these cells and those that migrated at greater Percoll densities. Amnion and chorion obtained after spontaneous labor had two major bands of cells. Estrone sulfatase was present in cells from both hands, whereas progesterone output from pregnenolone and prostaglandin F2 alpha metabolism predominated in the second band of cells with greater density. This pattern was particularly apparent in chorion. Dispersed cells from decidua tended to migrate throughout the gradient. In general, estrone sulfate to estrone conversion predominated in lighter cells whereas progesterone output from pregnenolone and prostaglandin F2 alpha metabolism predominated in cells of greater density. The output of progesterone from pregnenolone was significantly lower in cell preparations from chorion and decidua at spontaneous labor compared with cesarean section. We conclude that human amnion, chorion, and decidua contain distinct cell subpopulations based on Percoll migration and that in the membranes these change between cesarean section and spontaneous labor. Partial separation of estrone sulfatase from 3 beta-hydroxysteroid dehydrogenase and prostaglandin F2 alpha metabolizing activities has been demonstrated, which raises the possibility of paracrine interactions in vivo.

Cells, Cultured↗
PubMedDate not supplied

Distribution of annexin I and II in term human fetal membranes, decidua and placenta.

Annexin I and II are calcium binding proteins implicated in the regulation of a number of cellular functions, including secretory processes, prolactin release and prostaglandin formation. The cellular distribution of these proteins was examined in human term placenta, fetal membranes (amnion and chorion laeve) and decidua using immunohistochemistry. Annexin I was found in amnion epithelial cells and chorion laeve trophoblast but not in decidua, and was located in the syncytiotrophoblast cells of placenta. Annexin II and annexin II light-chain were located in the amnion epithelial cells, the cells of the mesenchymal layer between the amnion and chorion laeve trophoblast and endothelial cells lining the blood vessels in the decidua. In contrast to annexin I, annexin II was located in the villous core and not the syncytiotrophoblast cells in the placenta. There was no apparent change in the distribution of these annexins during labour. These findings indicate that the cellular distribution of these annexins is different, and may be an important consideration when examining their synthesis or action in tissues and in vitro with mixed cell populations and tissue homogenates.

Annexin A1↗
PubMedDate not supplied

Abnormalities of the fetal heart rate in preterm deliveries are associated with acute intra-amniotic infection.

OBJECTIVE: To evaluate whether fetal heart rate (FHR) patterns obtained in nonstress testing within 24 hours of delivery in patients with preterm delivery were associated with histologic acute infection, and if so, whether the associations are with maternal as opposed to fetal acute inflammation (acute amnionitis versus acute umbilical vasculitis). METHODS: The data set included 351 consecutive patients delivering from 22 to 32 weeks' gestation (excluding cases of preeclampsia; nonhypertensive abruption; stillbirth; fetal structural and karyotypic anomalies; Rh isoimmunization and hydrops fetalis; and maternal diabetes and hypertension). Severe variable decelerations were defined as FHR < 70 beats per minute lasting > 60 seconds, and decreased fetal heart variability included both reduced beat-to-beat variability and long-term heart rate cyclicity. Amniotic fluid volume was graded sonographically as part of a fetal biophysical profile. Acute inflammation of amnion (indicative of maternal inflammation) and umbilical cord (fetal inflammation) were scored by a single pathologist blinded to clinical data. RESULTS: Severe FHR variable decelerations were directly related to acute amnionitis (P = .012) and acute umbilical vasculitis (P = .0013). In preterm labor, decreased FHR variability was related to acute amnionitis (P = .005). All observations were independent of amniotic fluid volume or use of tocolytic agents. CONCLUSIONS: Severe variable decelerations and decreased FHR variability at < 32 weeks' gestation are related to histologic evidence of acute inflammation.

Adult↗
PubMed2001

Expression of erythropoietin mRNA, protein and receptor in ovine fetal membranes.

Erythropoietin and its receptor have been identified in human, murine and ovine placentas. Based on the common embryonic origin of the placenta and fetal membranes, we postulated that erythropoietin is similarly expressed in the fetal membranes. Using in situ hybridization and immunohistochemistry, we tested the hypothesis that ovine fetal membranes are sites of erythropoietin production and action. At 86, 103 and 138 days gestation, erythropoietin mRNA and protein were present in the amnion localized to the cell layer consisting largely of amniotic epithelium and in the chorion localized to the chorionic columnar cells consisting of cytotrophoblasts. Binucleate cells, differentiated cytotrophoblasts known to produce hormones, were identified in the chorion in the region of erythropoietin expression but were not observed in amniotic tissue. The erythropoietin receptor protein was present in the amnion and chorion at 103 and 138 days gestation but was not observed in either tissue at 86 days. In summary, erythropoietin appears to be produced as well as utilized within the ovine amnion and chorion. Within the amnion, the amniotic epithelial cells express the erythropoietin gene whereas, within the chorion, either the cytotrophoblasts or the binuclear cells may be the source. Due to the presence of the receptor, we speculate that the erythropoietin produced in the membranes may mediate fetal membrane function and/or growth through an autocrine and/or paracrine mechanism. Further, the fetal membranes may be the source of erythropoietin in the amniotic fluid.

Animals↗
PubMed2002

Implantation in the nine-banded armadillo: how does a single blastocyst form four embryos?

In the course of a study on reproduction in the nine-banded armadillo, conceptuses between the beginning of implantation and primitive streak formation were examined to determine the manner of trophoblast differentiation during invasion of the endometrium and the sequence involved in formation of four identical quadruplets. The armadillo blastocyst implants in the fundic recess of the uterus. A single amnion and cup-shaped epiblastic plate are formed, and an exocelom develops between the amnion and trophoblast of the implantation site. Loss of the abembryonic trophoblast exposes both visceral and parietal endoderm to the uterine lumen, inverting the yolk sac. Continued expansion of the exocelom facilitates the intrusion of the forming conceptus into the uterine lumen and is accompanied by enlargement of the epiblastic plate. Separate areas of condensations of epiblast cells are the first indication of formation of the four identical quadruplets. The single layer of microvillous trophoblast with basal infoldings (designated absorptive trophoblast) is most likely to contribute extensively to movement of fluid into the exocelom. The resulting expansion of the exocelom not only enlarges the implantation site but also displaces the collapsing common amnion, limiting the amnion to the areas of the forming embryos.

Animals↗
PubMed1995

Maternal, placental, and neonatal associations with early germinal matrix/intraventricular hemorrhage in infants born before 32 weeks' gestation.

This study tests the hypothesis that histologic placental lesions were significantly related to incidence of early or late germinal matrix/intraventricular hemorrhage (GM/IVH) in infants of less than 32 weeks' gestation independent of maternal or neonatal factors. Maternal and neonatal charts of 406 singleton liveborn nonanomalous infants born at less than 32 weeks' gestation were studied retrospectively for principal indication for delivery, delivery mode, timing of antenatal steroid treatment, diagnosis of labor and augmentation, tocolysis, fetal presentation, and umbilical arterial and venous blood gas values. Extracted from neonatal charts were gestational age, growth measurements, initial hematocrit and white blood cell count, administration of surfactant, and in the first 3 days of life, the use of pressor agents and volume expansion, lowest blood pressure, and data pertinent to respiratory function. Placental histologic examination was reviewed for various lesions, including histologic acute inflammation (graded on a scale of 0 to 4). GM/IVH (grades 1 to 4) diagnosed ultrasonographically less than 72 hours after birth was "early." GM/IVH diagnosed after 72 hours of life was defined as "late." Of the 406 patients, 44 (10.8%) had early GM/IVH; 21 (4.9%) had late GM/IVH. Stepwise logistic regression selected five factors independently related to increased early GM/IVH risk: Histologic acute inflammation (p < 0.002); gestational age in days (p = 0.053); antenatal steroid treatment less than 48 hours before birth (p < 0.035); volume expansion in the neonate (p < 0.30), and magnesium sulfate tocolysis (p < 0.025). Stepwise regression analysis considering the grade of GM/IVH changed the order of variables, with gestational age and use of pressor therapy being more strongly related to higher grade of GM/IVH than amnion inflammation. Delivery mode, presentation, principal indication for delivery, presence/augmentation of labor, mean biophysical profile scores, mean umbilical arterial and venous blood gas values, and surfactant therapy were not related to early GM/IVH in univariate or multivariate analyses. Neonatal factors associated (p < 0.05) with amnion inflammation were volume expansion at delivery and in the first 3 days of life, low mean systolic pressure, low mean oxygen pressure, low initial hematocrit and cord pH, and increased initial WBC and toxic granulations of neutrophils. Only gestational age, and no maternal or placental factors, was significantly related to late GM/IVH. Infants who have placentas with acute amnion inflammation and receive volume expansion, born to mothers who receive less than 48 hour's exposure to antenatal steroids and are selected to receive magnesium sulfate tocolysis, have increased incidence of early but not late GM/IVH. Amnion inflammation is significantly related to early GM/IVH and with early neonatal abnormalities in oxygenation, perfusion, and effective blood volume. Intra-amniotic infection leads to advanced preterm labor, which is unresponsive to tocolysis because of the inflammation. Intra-amniotic inflammation may sensitize the fetus to postpartum stresses or initiate early GM/IVH in utero via cytokine effects on cardiovascular instability.

Cerebral Hemorrhage↗
PubMed1984

[Premature membrane rupture: effect of intracervical PGE2 gel administration on plasma oxytocin, PGFM and PGEM levels in mother and child].

Premature rupture (= PR) of the amnion is a serious complication even for the mature child if it occurs earlier than 24 hours before birth. To keep the interval as short as possible, the authors induce labour from week 35/0 in case of PR, provided the Bishop score is greater than 7. If the bishop score is lower, they conduct intracervical priming of the cervix with 0.4 mg PGE2 gel before induction of labour. This has proved clinically superior to intravenous procedures. In the study presented here, the authors attempted to find out whether intracervical administration of PGE2 gel would result in changes in the maternal and foetal plasma concentrations of oxytocin, PGFM, or PGEM when comparing conditions in case of ruptured amnion with those if the amnion remained intact. If the amnion is intact and the cervix immature (less than 2 cm), intracervical administration of 0.4 mg PGE2 gel produces a significant OT increase within 30 minutes. From a cervical width of 2 cm onwards, the OT levels are already primarily enhanced and will hardly change even after PGE2 gel administration. Similar conditions obtain in PR. PGFM plasma levels will rise only slightly within an hour after intracervical PGE2 gel administration, independent of whether there has been a rupture or not, or whether the cervix is dilated less than 2 cm or 2 cm and more.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1999

Evidence for infection of the human embryo with adeno-associated virus in pregnancy.

Previous reports have demonstrated the presence of DNA of the human helper virus-dependent adeno-associated parvovirus (AAV) in uterine tissue and curettage material from early miscarriage. To examine infection of embryonic tissue during pregnancy, amnion fluids were analysed for the presence of AAV. Using polymerase chain reaction, AAV DNA was detected in 64 out of 238 DNA samples extracted from amnion cells. DNA of helper viruses were found in 12% (papillomavirus) and 18% (cytomegalovirus) of the samples (double infections with AAV in eight and nine cases, respectively). Furthermore, infectious AAV virions were found in 13 out of 43 AAV DNA-containing samples. In mothers with AAV DNA-positive amnion fluids, premature amniorrhexis and premature labour occurred significantly more frequently (P < 0.001). Using an immunofluorescence assay, 24% of newborn sera (unrelated to the amnion fluid samples) were found to contain IgM antibodies to AAV, in most cases paralleled by IgM antibodies in the mother's sera. The data demonstrate that AAV infection can occur in utero at early and at late stages of pregnancy. The observed complications at delivery should encourage studies to clarify possible pathological consequences of AAV infection in pregnancy and a possible latent infection of the fetus.

Amniotic Fluid↗
PubMed2003

Epithelial cell-derived neutrophil-activating peptide-78 is present in fetal membranes and amniotic fluid at increased concentrations with intra-amniotic infection and preterm delivery.

Intra-amniotic secretion and abundance of epithelial cell-derived neutrophil-activating peptide (ENA)-78, a potent chemoattractant and activator of neutrophils, was studied in the context of term and preterm parturition. Staining of ENA-78 immunoperoxidase was localized predominantly to chorionic trophoblasts and amniotic epithelium in term and preterm gestational membranes, with weaker and less consistent staining in decidual cells. The abundance of ENA-78 in membrane tissue homogenates was significantly increased ( approximately 4-fold) with term labor in amnion (n = 15), and with preterm labor ( approximately 30-fold) in amnion and choriodecidua (n = 31). In amnion tissue homogenate extracts, ENA-78 levels were positively correlated with the degree of leukocyte infiltration (r2 = 0.481). In amniotic fluids, median ENA-78 levels from pregnancies with preterm labor without intra-amniotic infection were significantly lower (P < 0.01 by ANOVA) than those from pregnancies with preterm deliveries with infection; levels in samples derived from term pregnancies were similar before and after labor. Production of ENA-78 by amnion monolayers was stimulated in a concentration-dependent fashion by both interleukin-1beta and tumor necrosis factor alpha. Production of ENA-78 by choriodecidual explants was increased modestly after 2-4 h of exposure to lipopolysaccharide (5 microg/ml). An immunoreactive doublet ( approximately 8 kDa) was detected in choriodecidual explant-conditioned media by immunoblotting. We conclude that ENA-78, derived from the gestational membranes, is present in increased abundance in the amniotic cavity in response to intrauterine infection and, hence, may play a role in the mechanism of infection-driven preterm birth and rupture of membranes secondary to leukocyte recruitment and activation.

Amniotic Fluid↗
PubMed1993

Origin of CA125 and SCC antigen in human amniotic fluid.

Levels of CA125 and SCC antigen in amniotic fluids were examined in 26 cases. All samples showed high levels of CA125 and SCC antigen. Statistically significant decreases in CA125 (p < 0.05) and increases in SCC antigen (p < 0.01) from the second to the third trimesters were recognized. We focused on amnion cells as likely sources of the 2 tumor markers in amniotic fluid. Analysis of in vitro culture of amnion cells and amniotic membranes revealed an accumulation of CA125 and no accumulation of SCC antigen in the culture supernatant. A Northern blot analysis using a cDNA probe of SCC antigen ensured that there was no mRNA expression of SCC antigen in the amnion, the cord or the placenta. It is likely that the amnion is a major source of CA125 in amniotic fluid, and that the fetus is the origin of SCC antigen.

Amniotic Fluid↗