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PubMed1990

Cyclic guanosine monophosphate metabolism in human amnion cells trisomic for chromosome 21.

An extra copy of chromosome 21, a small chromosome or a specific segment of it, is the cause of the disorder known as Down's syndrome (DS). Genes mapped to this chromosome include superoxide dismutase-1 (SOD-1) along with other enzymes. Gene dosage effects have been shown for some of these enzymes, including SOD-1. Increased SOD-1 has been suggested to stimulate the cGMP-forming enzyme, guanylate cyclase (GC). In the present study we have used amnion cells from DS subjects and normal subjects in order to indirectly test the effects of SOD-1 on the cGMP metabolism. We have measured the cAMP and cGMP content, SOD-1 activity, GC activity and cGMP phosphodiesterase (G-PDE) activity in amnion cells from DS subjects and normal subjects, respectively. The levels of cGMP in DS amnion cells were lower than in normal cells, although the SOD-1 activity was higher in DS amnion cells. Furthermore, the GC activity and the G-PDE activity were found to be lower in the trisomic cells. Our results do not support the suggestion that SOD-1 has a stimulatory effect on the GC activity.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1994

Urinary trypsin inhibitor has a protective effect on the amnion.

Urinary trypsin inhibitor-related substance (UTI-R) was measured in the amniotic fluid (n = 30), first neonatal urine (n = 10), meconium (n = 10), and adult urine (n = 10). The concentration of UTI-R excreted in the neonatal urine was significantly higher than in adult urine and meconium. Positive immunostaining for UTI was observed in amnion, umbilical cord and placenta. The effect of UTI was studied on the amnion using fura-2-acetoxymethyl ester. Interleukin-1 beta (IL-1 beta) and tumor necrosis factor-beta (TNF-beta) led to a significant increase in relative fluorescence release (RFR) of fura-2 (p < 0.05 and p < 0.02, respectively) while endotoxin did not show significant changes of RFR of fura-2. The effect of IL-1 beta and TNF-beta was almost abolished after incubation of UTI with the amnion cells (p < 0.03). This suggests that UTI may have a protective effect on the amnion especially against IL-1 beta and TNF-beta.

Amnion↗
PubMed1992

Effect of smoking on fibronectin production by human amnion and placenta.

Fibronectin production from amnion and placental tissues was evaluated in pregnant woman smokers and nonsmokers in order to examine if there were alterations of fibronectin metabolism in intrauterine tissues. In both amnion and placental tissues, cycloheximide inhibited the fibronectin output indicating that it was being synthesized. Mean fibronectin output by amnion in pregnant woman smokers was significantly lower than that in pregnant woman nonsmokers. In contrast, in the placenta from pregnant woman smokers, the output was significantly higher than that in pregnant woman nonsmokers. The present observations indicate that smoking alters an important biochemical constituent in amnion and placenta, possible leading to some complications.

Amnion↗
PubMed1987

Stimulation of prostaglandin E production in superfused human amnion by human amniotic fluid.

We studied the effects of human amniotic fluid (HAF) on the production of prostaglandin E (PGE) by amnion tissues using a technique of fresh-tissue superfusion. The production of PGE was linear with time for 4.5 h by amnion tissues superfused either with medium alone or with medium plus HAF (30% v/v). Tissues superfused with medium plus HAF produced significantly more PGE than tissues superfused with medium alone. Additionally, amnion tissue obtained at cesarean section, prior to labor, displayed a greater responsiveness to HAF than did amnion obtained after spontaneous labor.

Amnion↗
PubMed1975

Human amnion and lung tissue culture systems for possible detection and study of human RNA tumor viruses.

A human lung and an amnion cell line were identified as highly susceptible to transformation by the rhabdomyosarcoma-114 (RD-114) virus pseudotype of murine sarcoma virus (MSV). MSV transformation on these two cell lines demonstrated a) "one-hit" kinetics with an MSV stock which contained a 100-fold excess of MSV over its detectable associate RD-114 helper virus and b) only a slight increase (2X) in focus-forming titers by the addition of optimal concentrations of RD-114 helper virus. These findings indicated that the primary MSV interaction with those amnion and lung cells was that of non-productive transformation; and this was confirmed by the isolation of sarcoma-positive leukemia (helper) virus-negative (S+Lminus) cells from cloned terminal foci of MSV transformed human amnion and lung cells. These MSV-susceptible human cell lines are the first human cells identified as capable of demonstrating the defective nature of MSV. Human candidate oncornaviruses have not, however, been detected to date with the use of normal lung and amnion cells and their S+Lminus derivatives as indicator systems. These cell lines were useful for the isolation and identification of a new RD-114-like virus from a cat cell line.

Amnion↗
PubMed1989

Adenosine triphosphate activates the phospholipase-C cascade system in human amnion cells without increasing prostaglandin production.

Human amnion is hypothesized to be a target tissue for hormone messages from the fetus regarding labor. We have previously demonstrated prostaglandin E2 (PGE2) release in amnion after treatment with phorbol and oxytocin, but other potential agonists of the inositol phospholipid/protein kinase-C system have not been investigated. The effects of extracellular ATP on cytosolic calcium concentration [( Ca2+])i) inositol phosphate (IP) accumulation, and PGE2 production were studied in cultured human amnion cells. Intracellular free calcium [Ca2+]i was measured using the fluorescent dye fura-2. Addition of 0.01-30 microM ATP resulted in a [Ca2+]i transient which peaked within 15 sec and returned to baseline over 10 min. UTP (1 microM) was more effective than ATP (1 microM); [Ca2+]i levels rose from 233 to 2880 nM (UTP) and 2320 nM (ATP). A reduced effect was observed with other nucleotides in a rank order of agonist potency of ITP greater than CTP greater than ADP greater than GTP greater than TTP. No effect was seen with AMP, cAMP, or adenosine. This is consistent with P2 purinoceptors, as described in other tissues. ATP (100 microM) also dramatically increased IP accumulation. Inositol triphosphate, inositol bisphosphate, and inositol monophosphate were increased 7-, 9-, and 16-fold respectively. The agonist potency order of other nucleotides for IP accumulation was the same as that of [Ca2+]i. Pharmacological concentrations of ATP (1 mM) were required to increase PGE2 production. Many other nucleotides were equally effective at this concentration. ATP activates the phospholipase-C system in human amnion, as demonstrated by the increase in [Ca2+]i and inositol phosphates. The physiological significance of purinergic stimulation of this tissue remains unclear.

Adenosine Triphosphate↗
PubMed1995

Glucocorticoids stimulate the expression of prostaglandin endoperoxide H synthase-2 in amnion cells.

Corticosteroids increase the production of prostaglandin E2 (PGE2) and the activity of prostaglandin endoperoxide H synthase (PGHS) in cultured amnion cells, although they inhibit prostanoid biosynthesis in numerous other cell types. This suggests that glucocorticoids control the level of PGHS in amnion cells by a hitherto unexplored, positive regulatory mechanism. We have tested the possibility that corticosteroids act by stimulating the expression of messenger RNAs (mRNAs) encoding one or both isoforms of PGHS. Ribonuclease protection assays were used to determine the levels of PGHS-1 and -2 mRNAs and, for reference, gamma-actin mRNA levels in confluent primary cultures of human amnion cells. In untreated cultures, PGHS-1 and -2 mRNA levels were low, often not reaching the level of detection. Dexamethasone (DEX) treatment for 4 h resulted in a measurable level of PGHS-2 mRNA, which increased further 10-fold and 20-fold after incubation with the glucocorticoid for 8 h and 16 h, respectively. The stimulation was dependent on DEX concentration, and was concomitant with an increase in the capacity of the cells to metabolize arachidonic acid to PGE2. PGHS-1 mRNA levels remained low in DEX-treated cells, while the gamma-actin message level showed no change. Estradiol and progesterone had no influence on PGHS-2 mRNA expression, but cortisol increased the PGHS-2 mRNA abundance. The glucocorticoid antagonist RU486 blocked the effect of DEX. Conditioned media of DEX-treated cells did not contain steroid-induced factor(s) stimulating PGE2 production. Inhibition of protein synthesis by cycloheximide potentiated the effect of DEX, and raised the abundance of PGHS-1, PGHS-2, and gamma-actin mRNAs in untreated cells. DEX did not affect the stability of the PGHS-2 mRNA. These results show that glucocorticoids promote PGE2 synthesis by amnion cells by stimulating the expression of PGHS-2 mRNA in a receptor-dependent, selective, and immediate fashion.

Amnion↗
PubMed2000

Complementary mechanisms of enhanced oxytocin-stimulated prostaglandin E2 synthesis in rabbit amnion at the end of gestation.

The up-regulation of oxytocin (OT) receptors in rabbit amnion at the end of gestation is associated with a large increase in the ability of OT to stimulate PGE2 synthesis. The purpose of these investigations was to determine what other factors contribute to this increase. OT enhanced PGE2 synthesis at several levels. The concentrations of cytosolic phospholipase A2, which generates arachidonic acid for PGE2 synthesis, and PGH endoperoxide synthases (types 1 and 2), which catalyze the conversion of arachidonic acid to prostanoids, rose substantially in rabbit amnion at term. OT stimulated translocation of cytosolic phospholipase A2 to the cell particulate fraction, presumably by a Ca2+-mediated process, and phosphorylation of cytosolic phospholipase A2 via the extracellular regulated protein kinase 2/1-mediated pathway. OT-stimulated increases in intracellular Ca2+ concentrations and extracellular regulated protein kinase 2/1 phosphorylation were both mediated by G(q/11) activation. OT also increased the expression of PGH endoperoxide synthase-2 after treatment of amnion cells in culture for 2 h; however, PGE2 release in response to OT was virtually immediate. These findings show that the rapid stimulation of PGE2 synthesis by OT occurs through cytosolic phospholipase A2 activation and PGH endoperoxide synthase-1 activity, both of which, along with OT receptor concentrations, are considerably up-regulated in the amnion at the end of gestation.

Amnion↗
PubMed2004

Paradoxical proinflammatory actions of interleukin-10 in human amnion: potential roles in term and preterm labour.

IL-10 is regarded predominantly as an inhibitor of cell-mediated inflammatory reactions. As such, it has been suggested that IL-10 could have therapeutic potential, including the treatment of preterm labor. Using explant cultures of gestational membranes we have found that IL-10 does indeed exert anti-inflammatory properties in choriodecidua, but that in the adjacent amnion it has remarkable pro-inflammatory actions. Amnion prostaglandin (PG) E(2) production was significantly increased following 24-h treatment with IL-10 (5-100 ng/mL). Production of IL-8 also showed a significant stimulation at 100 ng/mL IL-10. In contrast, choriodecidual production of IL-8 and tumor necrosis factor (TNF)-alpha was dramatically inhibited by IL-10, confirming the ability of this tissue to exhibit a classical IL-10 response. IL-10 retained its stimulatory actions on amnion in the presence of IL-1beta and TNF-alpha stimulation. These findings suggest that the fetal membranes can exhibit opposing responses to IL-10, depending on whether the inflammatory insult occurs at the maternal or fetal face. While inflammatory reactions are negatively regulated by IL-10 in choriodecidua, if the pathogen reaches the amnion and threatens the fetus, pro-inflammatory reactions may predominate to ensure successful labor to spare and protect the fetus.

Amnion↗
PubMed1986

Stimulation of creatine kinase activity by calcium-regulating hormones in explants of human amnion, decidua, and placenta.

We have used stimulation of the activity of the brain type creatine kinase (CK) isoenzyme as a response marker to examine the effects of vitamin D metabolites, PTH, and calcitonin in cultured explants of placenta, decidua, and amnion from normal human deliveries. We found a biological response to PTH in placenta and amnion and to vitamin D metabolites in all three tissues. In the amnion, CK activity increased 2.3-fold after 24 h of incubation in 2.5 nM 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], 3.8-fold when incubated with 12.5 nM 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] and 2.7-fold when incubated with 10 U/ml bovine PTH. In the decidua, 24,25-(OH)2D3, but not 1,25-(OH)2D3 or bPTH caused a 1.7-fold increase in CK activity. In contrast, the placenta responded to 1,25-(OH)2D3 with a 1.6-fold increase in CK activity and to bPTH, with a 1.7-fold increase but did not respond to 24,25-(OH)2D3. Bovine calcitonin (100 ng/ml) had no effect on CK activity in any of the three tissues. Nearly all CK in both the unstimulated and stimulated explants was the brain type isoenzyme. CK activity increased significantly between 1 and 4 h after hormonal treatment in all experiments. The enzyme activity rose steeply with dose and reached a significant increase, and usually a plateau, at hormone concentrations considered to be physiological in vivo. [3H]Thymidine incorporation into DNA increased in parallel to stimulation of CK activity in all experiments, except that PTH did not increase DNA synthesis in the placenta. PTH did cause an increase in cAMP production in explants of amnion (1.5-fold) and placenta (2.6-fold).

Amnion↗
PubMed1991

Protein kinase-C activation is required for oxytocin-induced prostaglandin production in human amnion cells.

In previous work we reported that oxytocin activates phospholipase-C (PLC) and increases prostaglandin E2 (PGE2) release in amnion. Whether either of the consequences of activation of PLC by oxytocin, activation of protein kinase-C (PKC) or increases in intracellular calcium, directly results in the production of PGE2 is unknown. Phorbol esters (PMA) and epidermal growth factor (EGF) are also known to increase PGE2 release from amnion. In some tissues these agents are capable of activating the PLC postreceptor cascade system. This study was undertaken primarily to explore the mechanism of oxytocin-induced PGE2 production in amnion and secondarily to determine whether common aspects of PGE2 production by oxytocin, PMA, and EGF include activation of PLC or subsequent steps in this cascade followed by new mRNA/protein production. Involvement of PLC was assessed by inositol phosphate (IP1) turnover. IP1 turnover was increased by oxytocin (2.99 +/- 0.31-fold; P less than 0.01), but not by EGF or PMA. PMA inhibited oxytocin-provoked IP1 turnover (P less than 0.05). PKC involvement was initially evaluated with two PKC inhibitors, H7 and staurosporine. Each inhibited PGE2 production by oxytocin as well as that by PMA and EGF in a dose-dependent fashion. With H7, the IC50 for all agents was 5 microM; the IC50 for staurosporine was 2 nM for PMA and oxytocin and 5 nM for EGF. Agonist-induced PGE2 production was also assessed in cells in which PKC activity had been tachyphylaxed with a high concentration of PMA (400 ng/mL for 48 h). In such cells oxytocin and PMA no longer stimulated (P less than 0.001) PGE2 production, but EGF-stimulated PGE2 production was only slightly reduced. PKC involvement is, thus, implicated for oxytocin and PMA. Other enzymes that are inhibited by H7 and staurosporine are implicated in the production of PGE2 caused by EGF. Although tachyphylaxed cells produced no PGE2 with oxytocin, oxytocin increased intracellular calcium to levels higher than those seen in control cells (435 +/- 102 vs. 286 +/- 1.2) Actinomycin-D (P less than 0.001) and cycloheximide (P less than 0.05) inhibited PGE2 production caused by oxytocin, PMA, and EGF. PGE2 production by oxytocin in human amnion cells proceeds by activation of PKC, followed by new protein and mRNA production. Further, in cells without PKC, oxytocin-induced calcium transients do not increase PGE2. The ability of EGF to stimulate PGE2 in cells with no PKC activity also establishes that PKC activation is not a common intracellular step in the induction of PGE2 production by all agents.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Exposure of human amnion to amniotic fluid obtained before labor causes a decrease in chorion/decidual prostaglandin release.

Prostaglandin (PG) production by fetal membranes has been implicated in the initiation of human parturition, but its regulation is not well understood. We used an in vitro system to study paracrine control of term, fetal membrane PG production. Using a modified Ussing chamber, full thickness fetal membranes with attached decidua were sealed into a chamber so that each hemichamber was a compartment for either the fetal (amnion) or maternal (chorion/decidua) side. Released PGs from maternal and fetal sides were then measured after exposure of the amnion to either buffer or amniotic fluid. We found that basal release of PGs from both the fetal and maternal sides was 2- to 3-fold higher in membranes obtained after labor compared to those obtained before labor. When amnion obtained after labor was exposed to amniotic fluid, we found a 3- to 5-fold increase in the net release of PGE2 from the amnion; however, the maternal side showed an unexpected relative decrease in PGE2 and PGF2 alpha release. This was a paracrine effect, since direct exposure of chorion/decidua to amniotic fluid caused increased release of the PG precursor, arachidonic acid. Direct transfer of radiolabeled PG from fetal to maternal side was minimal.

Amnion↗
PubMed2003

Inducing proliferation of human amnion epithelial and mesenchymal cells for prospective engineering of membrane repair.

OBJECTIVE: To prepare a tissue engineering approach to fetal membrane repair after premature rupture of the membranes (PROM) by characterizing the proliferation potential of human amnion epithelial and mesenchymal cells from preterm and term placenta in primary culture. METHODS: Amnion epithelial and mesenchymal cells from 15 preterm (23-36 week) and 27 term placentas collected at cesarean section were separated enzymatically, characterized immunohistochemically (anti-cytokeratin 18 and anti-E-cadherin, and anti-vimentin, respectively), and their ratio determined. Proliferation on tissue culture polystyrene (TCPS) or collagen in one medium and on TCPS in four different media after 14 days was measured photometrically and compared in preterm vs. term placenta. For statistical analysis the Mann-Whitney test was used. RESULTS: Preterm and term epithelial:mesenchymal cell ratios were 4.3:1 and 7.8:1. Term epithelial cells proliferated similarly on TCPS or collagen. Mesenchymal cells proliferated only with fetal bovine serum (FBS). Proliferation of term amnion cells in medium containing FBS, epithelial growth factor (EGF), insulin, transferrin and triidothyronine(T3) was significantly increased (p < 0.001) compared with the other three media, and percentage proliferation was slightly higher in preterm cells. CONCLUSION: Characterization of human amnion epithelial and mesenchymal cells identified the most potent proliferation-inducing medium yet. Studies of the wound-healing potential of these cells are needed, examining their behavior and proliferation on fibrin microbeads and other extracellular matrixes as the next step towards engineering membrane repair in PROM.

Amnion↗
PubMed1988

Prolactin stimulates creatine kinase activity and DNA synthesis in explants of human amnion.

To characterize the action of hPRL and human placental lactogen on the amnion, decidua and placenta, we examined the effects of these hormones on the brain type isozyme of creatine kinase in cultured explants of these tissues from normal deliveries. In the amnion, hPRL (1 mg/l) caused a 1.8-fold increase in creatine kinase specific activity in 24 h, whereas hGH (1 mg/l) or human placental lactogen (1 mg/l) had no effect; oPRL (1 mg/l) also caused a 2.5-fold increase in creatine kinase activity. Neither hPRL, human placental lactogen nor hGH had a significant effect on creatine kinase activity in the placenta or decidua. [3H]thymidine incorporation into DNA increased in parallel to the stimulation of creatine kinase activity. The predominant isozyme of creatine kinase in both the unstimulated and stimulated explants was the brain type isozyme. Creatine kinase activity in the amniotic tissue increased significantly 2 h after hPRL treatment and reached its highest value at 4 h. The enzyme activity in the amnion rose with increasing hPRL dose and showed a significant increase at physiologic concentrations as low as 0.01 mg/l. This study, therefore, provides evidence for biological action of prolactin in amniotic tissue, suggesting that the amnion is physiologically responsive to prolactin.

Amnion↗
PubMed1999

Concentrations of activin A, inhibin A and follistatin in human amnion, choriodecidual and placental tissues at term and preterm.

To investigate labour-associated changes in production of activin and related hormones by gestational tissues we prepared extracts from amnion, choriodecidual and placental tissues delivered at term before labour (TNL; n=15), at term after spontaneous labour (TSL; n=15) or preterm (PTD; n=31) and measured concentrations of inhibin A, activin A and follistatin by ELISA. Activin concentrations in placental tissues were significantly (Mann-Whitney U-test; P<0.05) elevated with term labour (pg/mg protein, median; 1313 vs 2591), but in the PTD tissues concentrations were lower than those delivered spontaneously at term (3650 vs 2649). Inhibin concentrations also increased with term labour in the placenta (480 vs 686), but paradoxically decreased in amnion (188 vs 64) and choriodecidua (657 vs 358). Little or no significant changes in follistatin concentrations were observed. Concentrations of all three proteins were significantly correlated between amnion and choriodecidual tissues, and were significantly correlated with each other in most tissues (Spearman's ranked correlation; P<0.05). The activin:inhibin ratio in term amnion and choriodecidual tissues was increased 2 to 3-fold (P<0.0005 by Mann-Whitney U-test) after term labour, with similar trends also observed in the activin:follistatin ratio in placental tissue. These data suggest that a modest increase in placental activin and inhibin production may occur with labour at term. In addition, an increase in activin bioactivity may occur with labour, potentiating any paracrine effects of activin during parturition. The data, however, do not support an association between increased intrauterine activin biosynthesis and preterm delivery.

Activins↗
PubMedDate not supplied

Amnion degeneration over fetal placental surface vessels possibly resulting from focal hypoxia: a case report.

The monoamnionic placenta of this twin gestation had focal amnion necrosis, but this was present only over the fetal surface vessels of one twin; this twin also developed cerebral atrophy. We hypothesize that this degeneration is due to a more severely reduced oxygen tension in its vessels. The placental amnion epithelium may undergo several degenerative processes, including amnion nodosum and changes due to meconium staining. Sonography had disclosed what appeared to be a dividing membrane, but this was not found at birth when monoamnionic twins with entangled cords presented. The amnion degeneration was present only over the large surface fetal vessels of the placenta of that twin who also developed central nervous system degeneration, and macrophage infiltration was confined to the same lesions. Focal hypoxia from entangling cords may have caused this defect.

Amnion↗
PubMedDate not supplied

Chorion nodosum: a placental feature of the severe early amnion rupture sequence.

A lesion of placental membranes and/or chorionic disc mesenchyme found in 4 of 13 cases of the limb-body wall complex (LBWC) and in 1 case of term extraamniotic pregnancy, named chorion nodosum (ChN), is described. All five ChN cases were associated with amniotic bands. Although grossly inapparent and histologically superficially similar to amnion nodosum, ChN is a distinct flat lesion located in the chorion denuded of amnion, occurring in different clinical settings, and most probably having a different pathogenesis, because it has bimodal gestational age distribution and occurs earlier in pregnancy when associated with LBWC, and only in the LBWC cases associated with amniotic bands. Therefore, not only oligohydramnios but also other factors involved in etiopathogenesis of LBWC are most probably operative in ChN, such as early vascular disruption, direct contact of the chorion denuded of amnion with fetal body, or a metabolic defect of fetal epidermis and amnionic epithelium. Prolonged severe oligohydramnios most probably plays main role in the pathogenesis of ChN in term extraamniotic pregnancy.

Abnormalities, Multiple↗
PubMed1995

The empty amnion: a sign of early pregnancy failure.

Between 6.5 to 10 weeks of gestation, the length of the amniotic cavity is similar to that of the embryo. It follows that by the time an amniotic sac is detectable sonographically, an embryo of equal length should also be visualized. Retrospective review of case records at our institution revealed 15 patients in whom the amnion was visualized in the absence of an embryonic pole during first trimester sonography (endovaginal and transvesical). Indications for sonographic examination included gestational age estimation, discrepant size and dates, or vaginal bleeding. The mean sac diameter for the 15 gestations ranged from 14 to 36 mm, corresponding to gestational ages of 6.1 to 9.5 weeks. Ages based on the last menstrual period ranged from 6.1 to 11 weeks. A yolk sac was identified in all cases in addition to the amniotic sac, but neither an embryo nor cardiac pulsations were observed. In 12 of the 15 cases the size of the gestational sac was greater than 16 mm, such that the absence of an embryo also met an accepted criterion for a failed pregnancy. Follow-up in all cases confirmed early pregnancy failure. In this series the demonstration of an "empty amnion" (visualization of an amnion but no identifiable embryonic pole) was always associated with pregnancy loss. The "empty amnion" sign is helpful as an additional finding confirming early pregnancy failure.

Abortion, Spontaneous↗