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PubMed1984

Inhibitory effects of dispersed human amnion cells on production rates of prostaglandin E and F by endometrial cells.

Dispersed cells were prepared from amniotic membranes obtained either by caesarean section near term before labor (CS) or after spontaneous vaginal delivery (SL) and from human endometrial curettings. The cells were maintained separately in primary culture for about 18 h. Production rates (PR) of PGE and PGF during incubation for 1 h in defined medium were determined when the cell-types were separate (n = 60) or combined (n = 27) and when endometrial cells were incubated in medium conditioned by CS amnion cells (n = 13) or SL amnion cells (n = 12). The PR of PGE by CS amnion cells was five times greater than that of PGF and there was a two-fold increase (p less than 0.01) in PGE but not PGF by SL cells. Co-incubation was associated with a 25-32% fall in PR of both PGE and PGF (p less than 0.01) compared to the sum from separately incubated cells when CS cells were used whereas values for co-incubated SL cells did not differ from controls. Conditioned medium from CS but not SL cells inhibited PGE and PGF output by 30% and 40% (p less than 0.01) respectively. These findings suggest that human amnion cells release an inhibitor of prostaglandin synthesis in endometrial cells.

Amnion↗
PubMed1993

Tumor necrosis factor alpha stimulates amnion prostaglandin biosynthesis primarily via an action on fatty acid cyclooxygenase.

The purpose of this study was to determine how tumor necrosis factor alpha (TNF alpha) stimulates prostaglandin E2 production in human amnion. Amnion cells were isolated from term placentae and grown to confluence in culture. Incubations were conducted in quadruplicate wells for 16 hours with TNF alpha and protein synthesis inhibitors cycloheximide and actinomycin D, or arachidonic acid, acetylsalicylic acid (ASA), or staurosporine or H7 which inhibit protein kinase C activity. Prostaglandin E2 (PGE2) was measured by radioimmunoassay and cellular protein determined. The stimulatory action of TNF alpha on amnion PGE2 production was blocked by protein synthesis inhibitors, and the addition of arachidonic acid always enhanced the stimulatory properties of TNF alpha. TNF alpha consistently induced more rapid recovery from ASA treatment, and protein kinase C inhibition attenuated the stimulatory effects of TNF alpha. These results suggest that the stimulatory action of TNF alpha on amnion PGE2 production is likely at the level of induction of fatty acid cyclooxygenase activity and is partially dependent upon activation of protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Transforming growth factor-beta potentiates epidermal growth factor-induced prostaglandin E2 production in amnion cells.

Primary cultures of human amnion cells and the amnion-derived cell line WISH were used to evaluate the hypothesis that transforming growth factor-beta (TGF-beta) can modulate epidermal growth factor (EGF)- induced prostaglandin E2 (PGE2) production. Cells were preincubated for 1 hr with TGF-beta (0.0001-10 ng/ml) and then incubated in the presence or absence of EGF (10 ng/ml) for 4 hrs. TGF-beta alone did not stimulate PGE2 synthesis at any dose examined. However, when primary cultures of amnion cells or WISH cells were preincubated with TGF-beta and then challenged with EGF, there was a potentiation of PGE2 production that was much greater than the additive values of TGF-beta or EGF alone. These data suggest that EGF-induced PGE2 production by amnion cells can be modulated by low concentrations of TGF-beta.

Amnion↗
PubMed1994

Cytokines released by granulocytes and mononuclear cells stimulate amnion cell prostaglandin E2 production.

Preterm labor is associated with histologic chorioamnionitis and intraamniotic infection. Chorioamnionitis is characterized by infiltration of the fetal membranes by granulocytes. In intraamniotic infection, white cells accumulate in amniotic fluid. Granulocytes and mononuclear cells have been shown to release products that stimulate prostaglandin E2 (PGE2) production by amnion cells. The aim of the present study was to identify some of these products. Cell-free supernatant obtained from formylmethionyl-leucyl-phenylalanine (FMLP)-activated granulocytes was subjected to size exclusion chromatography. The fractions obtained were analyzed for their stimulatory effect on PGE2 production by human amnion cells in culture. Two peaks of PGE2-stimulatory activity were found. The activity present in one of these was synergistic with interleukin-1 beta (IL-1 beta) in stimulating amnion cell PGE2 production and was found to contain mainly transforming growth factor-alpha (TGF-alpha) immunoreactivity. This cytokine originated at least in part from eosinophils. The PGE2-stimulatory activity present in the other peak contained IL-1 beta, epidermal growth factor (EGF), and tumor necrosis factor-alpha (TNF-alpha). The release of IL-beta, TNF-alpha, TGF-alpha, and EGF by granulocytes differed from that of mononuclear cells. We have previously shown that TGF-alpha and EGF are synergistic with IL-1 and TNF-alpha in enhancing amnion cell PGE2 production. The different pattern of prostaglandin-stimulatory cytokines released from different types of white cells suggest that the cells may potentiate each others' effects.

Amnion↗
PubMed1996

The induction of cyclooxygenase-2 (COX-2) in intact human amnion tissue by interleukin-4.

Infection is a major cause of preterm labor. Amniotic fluid from women in preterm labor associated with intrauterine infection contains increased concentrations of cytokines. The mechanism underlying this association may be a cytokine-mediated stimulation of amnion cell prostaglandin production. The biosynthesis of prostaglandins from arachidonic acid is regulated by the enzyme cyclooxygenase which exists in two forms; the constitutive form (COX-1) and the other mitogen inducible (COX-2). The purpose of this study was to evaluate the effect of the cytokine interleukin-4 (IL-4) on cyclooxygenase activity and PGE2 production in amnion. Amnion tissue was taken at caesarean section from term women not in labor and immediately incubated for 2 hours in media containing concentrations of IL-4 ranging from 1 to 100 ng/ml. An increase in both COX-2 enzyme and prostaglandin E2 (PGE2) production was observed for all concentrations of IL-4 greater than 25 ng/ml (P < 0.05, n = 8). No change in COX-1 was observed. Our data suggest that the cytokine IL-4 may be involved in the pathogenesis of premature labor by inducing COX-2 in amnion tissue resulting in increased production of PGE2 and subsequent myometrial activity.

Amnion↗
PubMed1996

Cyclosporin A inhibits prostaglandin E2 production by fetal amnion cells in response to various stimuli.

Use of cyclosporin A as part of an immunosuppressive regimen in pregnant transplant patients is not uncommon. Although successful pregnancies have been reported with the use of various immunosuppressive agents including cyclosporin A, the concern for fetal outcome still remains. Our purpose was to evaluate the effects of immunosuppressive cyclosporin A on prostaglandin E2 (PGE2) production by human fetal amnion. Amnion cells were isolated from term placentae obtained at elective cesarean section before the onset of labor. Cells were grown to confluence and then incubated for 16 hours with cyclosporin A (1-1000 ng/ml) in the presence and absence of interleukin 1 beta (IL-1 beta, 1 ng/ml), phorbol 12-myristate 13-acetate (PMA, 10(-7) M) and ionomycin (0.5 microM). PGE2 was measured by radioimmunoassay and cellular protein determined. IL-1 beta, PMA and ionomycin all stimulated amnion cell PGE2 production as expected. However, these stimulatory actions were attenuated by at least 50% when cells were co-incubated with cyclosporin A (1000 ng/ml). Concentrations of cyclosporin A tested included the therapeutic range (250-1000 ng/ml). Our results indicate that cyclosporin A does not stimulate amnion cell PGE2 production and is probably unrelated to preterm labor and delivery in allograft recipients.

Amnion↗
PubMed1990

A monokine stimulates prostaglandin-E2 production by human amnion.

The studies reported in this communication were designed to test the hypothesis that products of mononuclear cells are capable of stimulating prostaglandin E2 production by human amnion. Conditioned media obtained from peripheral blood mononuclear cells were incubated with amnion cells in primary culture. A dose dependent increase in PGE2 biosynthesis was observed in response to increasing amounts of the conditioned media. These observations suggest that mononuclear cells produce a factor(s) capable of stimulating prostaglandin production by amnion cells. The signal responsible for the increased biosynthesis of prostaglandins by human amnion associated with parturition in the setting of intraamniotic infection may be of host origin.

Amnion↗
PubMed1991

Synergistic stimulation of amnion cell prostaglandin E2 synthesis by interleukin-1, tumor necrosis factor and products from activated human granulocytes.

We examined the interactions between supernatant from FMLP-activated human granulocytes, recombinant interleukin-1 (IL-1) and recombinant tumor necrosis factor (TNF) in the stimulation of prostaglandin E2 (PGE2) production by human amnion cells. Amnion cells from elective term cesarian sections were cultured in monolayer culture. Human granulocytes were activated with FMLP and centrifuged to obtained cell-free supernatant. Amnion cells were treated with granulocyte supernatant, IL-1 alpha, IL-1 beta, TNF-alpha, TNF-beta, or different combinations of these. Each of the stimulators alone enhanced the PGE2 production 5- to 27-fold. Granulocyte supernatant was synergistic with each of the cytokines. The combinations of IL-1 alpha or IL-1 beta with either TNF-alpha or TNF-beta caused a synergistic stimulation of amnion cell PGE2 production as well, whereas the combinations of IL-1 alpha with IL-1 beta or of TNF-alpha with TNF-beta were not synergistic. Furthermore, granulocyte supernatant was synergistic with the combination of IL-1 and TNF, resulting in a more than 150-fold stimulation of PGE2 production. Indomethacin completely suppressed these effects. We propose that granulocyte products acting together with IL-1 and TNF enhance PGE2 synthesis during inflammation, and serve as signals for the initiation of preterm labor in the setting of intra-amniotic infection.

Amnion↗
PubMed1991

A product of activated human granulocytes stimulates prostaglandin E2 synthesis in human amnion cells.

Cell-free supernatant from formylmethionyl-leucyl-phenylalanine (fMLP)-activated granulocytes causes a time- and concentration-dependent stimulation of prostaglandin E2 (PGE2) production in amnion cells. PGE2 concentration in the culture medium after 36 h treatment with granulocyte supernatant (from 40 x 10(6) granulocytes/ml of amnion cell medium), 1.49 +/- 0.71 pg/ng DNA (n = 13), was significantly higher (p = 0.0015) than in control cells (0.33 +/- 0.23 pg/ng DNA, n = 13). Indomethacin abolished this stimulation. Granulocyte supernatant and human epidermal growth factor (hEGF) had an additive effect on amnion cell PGE2 production. Catalase, superoxide dismutase (SOD), protease inhibitors or the platelet-activating factor (PAF) antagonist L-659,989 had no effect. Actinomycin D, cycloheximide and mepacrine reduced the PGE2 production. The phospholipase A2 activity present in granulocyte supernatants was resistant to heating, whereas heating decreased their PGE2-stimulating activity by 92%. Exogenous phospholipase A2 had no effect on PGE2 synthesis. The granulocyte product could be precipitated with ammonium sulphate. On gel filtration of supernatant, two peaks of PGE2-synthesis stimulating activity were obtained (molecular weights 12,000 and 60,000). This data serve to explain the association of chorioamnionitis with preterm labor: activated granulocytes release a protein(s) that induces prostaglandin production in amnion cells, and thus promote labor.

Amnion↗
PubMedDate not supplied

Regulation of fetal fibronectin production in human amnion cells.

OBJECTIVE: We evaluated the role of human amnion in the production of fetal fibronectin and assessed the regulation of fetal fibronectin production by inflammatory products and cytokines. METHODS: Human amnion cells were grown in culture. At confluence, the cell were incubated with and without lipopolysaccharide, interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6. Fetal fibronectin production was measured in the supernatant fluid using an enzyme-linked immunosorbent assay technique. RESULTS: Unstimulated amnion cells produced fetal fibronectin, and production was increased by lipopolysaccharide, interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6. CONCLUSION: Human amnion cells in vitro produce fetal fibronectin in substantial quantities. This production is stimulated by inflammatory products and mediators that are considered to be important in the initiation of some cases of preterm labor.

Amnion↗
PubMed2004

Autologous amnion graft for repair of myelomeningocele: technical note and clinical implication.

OBJECTIVE AND IMPORTANCE: Amniotic membrane can be used as autologous reconstruction graft material when aseptically obtained. We introduce here a novel repair technique using autologous amnion graft, and report a case presentation of myelomeningocele successfully treated with this graft material. TECHNIQUE: Amniotic membrane, which was composed of amnion and chorion, was aseptically harvested at cesarean section. Removing chorionic tissue, amnion containing monolayer of amniotic epithelial cells and underlining fibrous tissue was isolated. After the procedure of reconstruction of neural and meningeal elements, the membrane was placed as onlay autograft over the reconstructed neural structure followed by suture of undermined skin flap without any myocutaneous flap transfer technique or fascial transposition from paraspinal muscles. RESULTS: The postoperative healing process of the wound was excellent. CONCLUSION: Autograft of amniotic tissue has no risks of rejection, foreign body reaction, or transmission of slow virus infection to reconstruct the lesion of newborn patient. Amnion autograft would be a biologic rationale to promote wound healing, being applied as a part of a variety of pediatric neurosurgical procedure.

Adult↗
PubMed1997

Changes in activity of cytosolic phospholipase A2 in human amnion at parturition.

OBJECTIVE: The purpose of this study was to determine whether increased cytosolic phospholipase A2 activity mediated arachidonic acid mobilization for prostaglandin synthesis in amnion at parturition. STUDY DESIGN: Amnion was collected immediately after delivery from four groups of patients: preterm (<37 weeks) with no labor or labor and term (>37 weeks) with no labor or labor and stored at -70 degrees C. Tissues were homogenized and centrifuged for 1 hour at 100,000 g, and cytosol was assayed for cytosolic phospholipase A2 activity with use of carbon 14-labeled 1-stearoyl-2 arachidonyl phosphatidylcholine plus 10 micromol/L unlabeled substrate and 5 mmol/L calcium in 10 mmol/L N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid, pH 7.4. Incubations were performed in duplicate +/- 10 micromol/L arachidonyl trifluoromethyl ketone, a specific inhibitor of cytosolic phospholipase A2 activity, at 30 degrees C for 45 minutes. RESULTS: Total cytosolic phospholipase A2 activity (in picomoles of arachidonic acid per minute per milligram of protein) calculated as the difference between the activity in the presence and absence of arachidonyl trifluoromethyl ketone was (mean +/- SE) as follows: preterm no labor (n = 7) 8.94 +/- 3.08, preterm with labor (n = 6) 6.79 +/- 2.31, term no labor (n = 7) 14.85 +/- 1.66, and term with labor (n = 5) 5.51 +/- 1.52. Enzyme activity increased with gestational age and was highest in the term no labor group. A significant decrease in cytosolic phospholipase A2 activity occurred with labor (p < 0.05). The greatest decrease in activity was in the term group (p < 0.05). CONCLUSION: Total cellular cytosolic phospholipase A2 activity in amnion is highest in anticipation of labor but during labor total activity is depleted, resulting in the low activity measured after delivery of the placenta. The substrate specificity and changes in amnion total cytosolic phospholipase A2 activity with labor strongly suggests a role in mediation of arachidonic acid mobilization and prostaglandin synthesis at labor.

Amnion↗
PubMed1998

Cytokine and prostaglandin production by amnion cells in response to the addition of different bacteria.

OBJECTIVE: Our goal was to evaluate the effect of Escherichia coli, Bacteroides fragilis, Mycoplasma hominis, and Staphylococcus aureus on cytokine and prostaglandin production by amnion cells in vitro. STUDY DESIGN: Amnion cells were obtained from women undergoing elective cesarean section before the onset of labor and cultured in a primary cell culture. Confluent amnion cells were incubated with heat-inactivated bacteria in different concentrations (10(1) to 10(6) colony-forming units/ml) for 48 hours. Samples for quantification of interleukin-1 beta, interleukin-6, interleukin-8, tumor necrosis factor-alpha, and prostaglandin E2 were collected at 6, 12, 24, and 48 hours. RESULTS: Under basal conditions, minor amounts of interleukin-6 and interleukin-8 were detectable. Incubation of amnion cells with E. coli enhanced the secretion of interleukin-8 and also induced an transient increase of prostaglandin E2 in a dose-dependent manner. B. fragilis produced an increase in the secretion of interleukin-6 and interleukin-8. M. hominis and S. aureus did not cause an increase in either interleukin-6, interleukin-8, or prostaglandin E2. CONCLUSION: The gram-negative bacteria E. coli and B. fragilis stimulated interleukin-6 and interleukin-8 to a greater degree than the other bacteria investigated in this study. This finding may be of clinical interest in the onset of preterm birth.

Amnion↗
PubMed1999

Immunohistochemical localization of the prostaglandin E subtype-1 receptor in cytokine-stimulated and unstimulated amnion cells.

OBJECTIVE: To visualize histochemically the prostaglandin EP1 receptor in human amnion cells and to study the effect of inflammatory cytokines, which are known to stimulate the EP1 receptor, on localization. METHODS: Immortalized amnion cells, grown on standard microscope slides and either nonstimulated (control) or stimulated by incubation in culture medium containing interleukin-1beta (25 ng/mL), interleukin-4 (50 ng/mL), or tumor necrosis factor alpha (25 ng/mL), were incubated with rabbit anti-human EP1 antibody and stained by a two-step indirect immunoperoxidase strepavidin-biotin method using horseradish peroxidase and 3,3' diaminobenzidine as the chromogen. The localization was done on ten different flasks of cells. Duplicate slides for each cytokine concentration were prepared. Negative controls for each reagent, prior blocking with 1% bovine serum albumin or 1% milk, or pretreatment with preimmune rabbit immunoglobulin G were run simultaneously. Slides were viewed by standard light microscopy with and without counterstaining with hematoxylin. RESULTS: Amnion cells incubated in medium alone showed receptor localization throughout the cytoplasmic region of the cell membrane. The localization was nonuniform; a discrete unipolar region of perinuclear nonlocalization was observed. Staining occurred in widely dispersed nests. Cytokine stimulation resulted in increased intensity of staining and an increase in the size of the positive nests; however, it did not affect the discrete unipolar perinuclear region of nonlocalization. CONCLUSION: Histochemical localization of the human EP1 receptor confirms a cytoplasmic identity and probable plasma membrane localization. Stimulation by inflammatory cytokines increases staining by recruitment of new amnion cells and appears to increase receptor density per cell.

Amnion↗
PubMedDate not supplied

Mechanism of interleukin-1 beta stimulation of human amnion prostaglandin biosynthesis: mediation via a novel inducible cyclooxygenase.

We have evaluated the mechanism by which interleukin-1 beta (IL-1 beta) increases amnion cell PGE2 production in a concentration-dependent manner. IL-1 beta-stimulated amnion cell PGE2 biosynthesis was time-dependent, and significant stimulation occurred within 2 h of incubation. IL-1 beta stimulation occurred in the presence of added arachidonic acid but was abrogated by treatment with cycloheximide and actinomycin D. Amnion cells treated with IL-1 beta recovered rapidly from aspirin pretreatment suggesting an action on fatty acid cyclooxygenase (COX). Increased amounts of COX protein were demonstrated by Western blot analysis within 2 h of IL-1 beta treatment of amnion cells. Northern blot analysis using a probe specific for a novel form of COX (COX-II) showed an increase in mRNA for this COX within 30 min. This finding using a homologous detection system and human cells of fetal origin in primary culture provides strong support for a physiological role for COX-II in man.

Amnion↗
PubMedDate not supplied

Characterization of antibodies to antigens of the human amnion.

The specificities of antisera produced in nine rabbits to seven different preparations of human amniotic epithelium and controls were studied by immunofluorescence on cryostat sections of human amniochorions, placentae and a large collection of other tissues. Three different groups of reaction patterns were identified with the use of these antibodies, indicating the presence of at least three antigenic groupings which have been tentatively designated as amnion antigens 1 (AA1), amnion antigens 2 (AA2) and amnion antigens 3 (AA3). The AA1 group was found on the ectodermal tissues of breast ductal and corneal epithelium as well as on Hassall's corpuscles, while the AA2 group was also found on breast ductal and corneal epithelium and basal keratinocytes, but not on Hassall's corpuscles. The AA3 group was found on basement membranes of ectodermally derived epithelium, but was negative on kidney. The identification of the distribution of antigens in common with ectodermal tissues and extra-embryonic membranes suggests that human amnion and chorion may have a close embryological relationship with embryonic ectoderm and its subsequent products of organogenesis.

Amnion↗
PubMed2000

The hydroxyproline content of amnion and prelabour rupture of the membranes.

OBJECTIVE: To determine whether prelabour rupture of the membranes is caused by a generalised reduction in amniotic collagen. SETTING: Leeds General Infirmary, UK. STUDY DESIGN: The hydroxyproline content of amnion from 55 women with prelabour rupture of the membranes was compared with that from 50 women whose membranes ruptured during labour and 28 women who were delivered by elective caesarean section. RESULTS: No association was found between hydroxyproline content and the timing of membrane rupture. Hydroxyproline content was inversely correlated with gestation. The hydroxyproline content per cm(2) amnion was significantly increased in cases which had laboured. There was a strong correlation between the mechanical properties and the hydroxyproline content of amnion. CONCLUSIONS: PROM is not associated with a generalised reduction in the hydroxyproline content of amnion.

Amnion↗
PubMed1997

Eicosanoid production by placental and amnion tissues from control and non-insulin-dependent diabetic rats. Influence of oxytocin in the incubating medium.

Eicosanoid production by intrauterine tissues from control and neonatal-streptozotocin induced diabetic rats during late pregnancy was evaluated. In diabetic placenta the release of 6-keto-PGF1alpha was found diminished when compared to controls. In addition, LTB4 generation was increased in diabetic placenta. No alterations in the production of TXA2, PGE2, PGE1 and PGF2alpha was found when diabetic and control placenta were compared. In amnion tissue a decreased generation of 6-keto-PGF1alpha was observed in the diabetic group, but no alteration in any other eicosanoid evaluated was found. Oxytocin (5 mU/ml, in vitro), which increases prostaglandin synthesis in rabbit and human amnion tissues, did not modify eicosanoid generation in control rat amnion. In contrast, in diabetic amnion the presence of oxytocin further decreased the release of 6-keto-PGF1alpha and diminished PGE1 generation. The present results suggest that this mildly diabetic state induces alterations in eicosanoid production in intrauterine tissues, abnormalities probably enhanced during parturition, when endogenous concentrations of oxytocin are elevated.

6-Ketoprostaglandin F1 alpha↗