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PubMed1999

The anchoring zone in the human placental amnion: bunches of oxytalan and collagen connect mesoderm and epithelium.

This study deals with the examination of the elastic fibre system as well as collagen fibrils and collagen type IV in the amnion of the human chorionic plate of uncomplicated pregnancies at term. In organs other than placenta, the elastic fibre system comprises elastic fibres, elaunin and oxytalan microfibrils. The investigation was performed by light and electron microscopy and immunocytochemistry. Abundant oxytalan fibres were present in all amnionic layers, while no elastic fibres were found. Oxytalan microfibrils formed a broad sub-epithelial layer and were intermingled with collagen fibrils in the subjacent compact layer and in the amnionic mesoderm. Light microscopically, bunches containing orcein-stained oxytalan and collagen-type-IV-immuno-stained microfibrils were seen rising from the amnionic mesoderm perpendicularly towards the epithelial layer, where they obviously inserted. It can be assumed that the subepithelial microfibrillar layer and the following compact layer form an anchoring zone between the amnionic mesoderm and the epithelium that may contribute to the maintenance of strength. The ultrastructure of the bunches clearly showed collagen fibrils mixed with oxytalan microfibrils. No collagen type I-immunostaining was found in the bunches. After pretreatment of cryostat sections with elastase, oxytalan-orcein-staining was absent, but collagen type IV-immunoreactivity was not altered. Furthermore, after oxytalan-orcein-staining resp. anti-collagen type IV incubation, all positive fibres revealed an identical morphological pattern. We propose that oxytalan and collagen type IV may represent further members of the microfibril complex.

Adult↗
PubMed1986

The effect of fetal urine on arachidonic acid metabolism in human amnion cells in monolayer culture.

Human amnion cells in primary monolayer culture were used as a model system to evaluate the regulation of arachidonic acid metabolism and prostaglandin E2 production in amnion. Amnion cells were incubated with carbon 14-labeled arachidonic acid, and after various times the distribution of radiolabeled arachidonic acid in the lipids of these cells were determined. After incubation for 72 hours, 91% of the total radiolabeled arachidonic acid incorporated into cellular lipids was present in glycerophospholipids, and 9% was present in neutral lipids. The formation of [14C]prostaglandin E2 from [14C]arachidonic acid was maximal after 8 hours. In these studies the effect of human fetal urine on arachidonic acid metabolism in these cells was investigated (the production of prostaglandin E2 by amnion cells is increased by treatment with fetal urine). In cells incubated with [14C]arachidonic acid in the incubation medium, treatment with fetal urine for 4 hours caused a threefold to fourfold increase in [14C]prostaglandin E2 production, yet there were no detectable differences in the content of [14C]arachidonic acid in specific glycerophospholipids or neutral lipids of the cells after such treatment. In other studies, amnion cells were preincubated for 72 hours with [14C]arachidonic acid, and thereafter the cells were treated with fetal urine for 24 hours. With fetal urine treatment the amount of [14C]arachidonic acid in triacylglycerols decreased significantly compared with that in nontreated cells, but the formation of [14C]prostaglandin E2 was not increased. Thus we suggest that in response to fetal urine, prostaglandin E2 is formed from arachidonic acid that is released from a highly specific, stimulus-sensitive lipid pool or else from arachidonic acid that is derived from extracellular sources.

Amnion↗
PubMed1990

Production of prostaglandin E2 by human amnion in vitro in response to addition of media conditioned by microorganisms associated with chorioamnionitis and preterm labor.

To examine the potential role of bacterial infection in the cause of spontaneous preterm labor, human amnion cells in tissue culture were exposed to medium conditioned by culturing each of 21 microorganisms previously found in association with chorioamnionitis and preterm labor. At a final concentration of 0.1% bacterial conditioned medium, a significant stimulation of prostaglandin E2 production from amnion cells was observed for this range of microorganisms. Conditioned medium obtained from culturing Bacteroides fragilis caused a dose-related increase in prostaglandin production, final concentrations of 0.02% to 0.1% being stimulatory but greater concentrations (0.1% to 10%) causing a progressive inhibition of prostaglandin synthesis. A similar concentration-related response in which stimulation was followed by inhibition occurred on addition of increasing concentrations of phospholipase A2 to amnion cells. These data suggest that bacterial phospholipase may release arachidonic acid from amnion leading to prostaglandin E2 synthesis, but excessive addition of phospholipase and consequent increased arachidonic acid availability may give rise to substrate inhibition of cyclooxygenase enzyme and inhibit prostaglandin E2 synthesis. Overall it appears that a wide variety of microorganisms associated with preterm labor may secrete phospholipase, which liberates amnion arachidonic acid for conversion to the oxytocic agent prostaglandin E2.

Amnion↗
PubMed1991

Morphologic changes in the human amnion epithelium that accompany labor as seen with scanning and transmission electron microscopy.

Scanning and transmission electron microscopy were used to assess the influence of normal, active labor on the ultrastructure of the human amnion epithelial membrane. Amnion membranes (reflected and placental portions) were obtained from patients either in active labor who were delivered vaginally or by cesarean section after 6 to 12 hours of labor or from patients who underwent elective cesarean section before clinical signs of overt labor. Scanning electron microscopy revealed that reflected amnion membranes that were obtained from patients who were not in labor consisted of a uniform single layer of epithelial cells with numerous microvilli on the apical surface and closely associated cellular borders. In contrast, amnion membranes that were obtained from patients who were in labor consisted of a single layer of epithelial cells, which was interrupted by wide intercellular gaps and extracellular extrusions. Transmission electron microscopy showed that intercellular junctions tended to be less complex in patients who were in labor versus patients who were not in labor. Although lipid droplets were prevalent in both patient groups, specimens that were obtained from patients who were in labor had more lipid droplets per cell than specimens from patients who were not in labor. These results support the theory that the complex biochemical events that culminate in parturition are accompanied and/or preceded by demonstrable morphologic changes in the amnion membrane.

Amnion↗
PubMed1991

Regulation of CA 125 production by amnion and WISH cells in culture.

Amnion and human amnion-derived WISH cells release CA 125 antigen into culture medium. CA 125 output was higher in WISH cells than in amnion cells. In this study we showed that release of the antigen is regulated, with both amnion and WISH cells responding in a similar manner to the tested agents. Release of CA 125 decreased in the presence of dexamethasone (10(-6) mol/L) or cycloheximide (0.1 micrograms/ml) and increased when colchicine (0.01 micrograms/ml) was added to the culture medium. Stimulatory and inhibitory effects were more apparent after 3 days in culture. The precise mechanisms by which some of these agents (colchicine and dexamethasone) affect CA 125 release remain unknown. We propose that amnion and WISH cells in culture represent a useful model to investigate some regulatory aspects of the production of CA 125 in normal tissues.

Amnion↗
PubMed1992

Decrease in annexin I messenger ribonucleic acid expression in human amnion with labor.

OBJECTIVE: Annexins are a superfamily of proteins that are thought to inhibit phospholipase A2 activity and hence inhibit prostaglandin production. The purpose of this study was to test the hypothesis that annexin I concentration in human amnion is reduced with labor and that this reduction is mediated by a decrease in annexin I messenger ribonucleic acid expression. STUDY DESIGN: Amnion and choriodecidua were collected from term singleton pregnancies, eight after spontaneous vaginal delivery and eight from elective cesarean section without labor. Annexin I protein was quantitated by Western blotting. Ribonucleic acid was isolated from amnion, and then annexin I messenger ribonucleic acid was identified by Northern hybridization and quantitated by slot blotting. RESULTS: Annexin I (35 kd) was identified in amnion tissue. The concentration in the group undergoing labor (320 +/- 45 integrated optical density units, mean +/- SE) was significantly reduced (p < 0.05) compared with that in the group not undergoing labor (635 +/- 65 units). The size of the annexin I messenger ribonucleic acid was approximately 1.8 kb. The mean integrated optical density for the labor group (840 +/- 139 units, mean +/- SE) was significantly reduced (p < 0.05) compared with that of the nonlabor group (1912 +/- 464 units). CONCLUSION: There is a significant decrease in annexin I messenger ribonucleic acid expression in human amnion with labor, corresponding to a significant decrease in annexin I protein concentration. This may contribute to the increased phospholipase A2 activity, arachidonic acid mobilization, and prostaglandin production at labor in humans.

Amnion↗
PubMed1995

Expression of parathyroid hormone-related peptide and its receptor messenger ribonucleic acid in human amnion and chorion-decidua: implications for secretion and function.

OBJECTIVE: Our purpose was to define the location and packaging of parathyroid hormone-related peptide in amnion-chorion and the potential target tissues for its action in fetal membranes. STUDY DESIGN: We studied fetal membranes by use of light microscopic immunocytochemistry with three monoclonal antibodies against distinct regions of the parathyroid hormone-related peptide molecule. For electron microscopy immunogold analysis with a monoclonal antibody specific to the 109-141 fragment was used to observe parathyroid hormone-related peptide intracellularly in amnion membrane and in the chorion layers. Multiplex reverse transcriptase-polymerase chain reaction with Southern blotting was used to identify parathyroid hormone/parathyroid hormone-related peptide receptor and control messenger ribonucleic acids in amnion and chorion-decidua. RESULTS: All monoclonal antibodies revealed immunoreactive parathyroid hormone-related peptide in the amniotic epithelial cells and in some fibroblast-like cells embedded in the extracellular matrix of the amnion. Parathyroid hormone-related peptide was also found in the chorion in fibroblast and trophoblast layers and in decidua. Ultrastructurally immunogold particles were evenly distributed throughout the amniotic epithelial cells and were present in apical microvilli and near the basal membranes. Electron microscopy studies of the chorion cytotrophoblast also showed freely dispersed immunogold particles of parathyroid hormone-related peptide with no packaging in secretory granules. Low to undetectable levels of parathyroid hormone/parathyroid hormone-related peptide receptor messenger ribonucleic acid were found in amnion tissue, whereas abundant receptor messenger ribonucleic acid was found in chorion-decidua. CONCLUSIONS: These results suggest the presence of a parathyroid hormone-related peptide paracrine system within the human fetal membranes.

Amnion↗
PubMed1989

Interleukin-1 stimulates prostaglandin biosynthesis by human amnion.

The purpose of these studies was to determine if Interleukin-1 (IL-1) alters the rate of prostaglandin biosynthesis by human amnion. Primary monolayer cultures of amnion cells were established from women undergoing elective cesarean section before the onset of labor. Natural purified and recombinant human IL-1 alpha and IL-1 beta were incubated with amnion cells in culture, and prostaglandin E2 (PGE2) biosynthesis was measured by radioimmunoassay in cell-free media. A concentration-dependent increase in PGE2 production by amnion cells occurred in response to natural purified and recombinant IL-1 preparations. No differences in the parameters of the dose-response curves between the two IL-1 gene products could be determined (p greater than 0.05). Indomethacin blocked the effect of IL-1 in prostaglandin biosynthesis by human amnion. Interleukin-1, a fever mediator, could serve as a signal for the initiation of labor in cases of intrauterine or systemic infection.

Amnion↗
PubMed1990

Increased and intermittent prostaglandin release from amnion detected by a new superfusion technique for full thickness fetal membrane.

Prostaglandin E2 (PGE) and F2 alpha (PGF) release by the intact fetal membranes is described using a novel superfusion technique allowing for the independent assessment of prostaglandin release from the amnion and chorio-decidua whilst maintaining the anatomical integrity of the fetal membranes. The effect of labour on prostaglandin release is described. Using this system it was confirmed that the amnion is a major site of prostaglandin release and possibly production. Labour resulted in a significant increase of both PGE and PGF release from the amnion side only (Pre-labour: PGE 918 pg/cm2/3h, PGF 370 pg/cm2/3h; Labour: PGE 2993 pg/cm2/3h, PGF 662 pg/cm2/3h). No change in either PGE or PGF release from the chorio-decidual side was observed in relation to labour. In addition a change in the pattern of prostaglandin release from the amnion was observed in tissues obtained after the onset of labour. In 6 of 8 samples obtained after spontaneous labour an intermittent or pulsatile release of both PGE and PGF was observed from the amnion side as compared to the steady state of prostaglandin release from all 10 samples obtained before labour.

Amnion↗
PubMed1981

In vitro production of prostaglandins E, F, and 6-keto prostaglandin F1 alpha by human pregnant uterus, decidua and amnion.

The production of prostaglandins (PGs) E and F and 6-keto PGF1 alpha was investigated by using human decidua, amnion, and pregnant myometrium obtained before and after onset of labor, and human nonpregnant myometrium collected during luteal phase. PGs produced were measured by radioimmunoassay developed in our laboratory. The radioimmunoassay for 6-keto PGF1 alpha is specific and accurate. PGE was formed at an almost constant rate regardless of the condition under which the three tissues tested were obtained, with the amnion showing the highest activity compared with decidua and myometrium. PGF production increased remarkably during labor in the myometrium and decidua but not in the amnion. In the myometrium during labor, PGF levels were three times higher than before labor. The pregnant myometrium produced more PGs than the nonpregnant myometrium. The production of 6-keto PGI1 alpha, a stable, non-enzymatically formed derivative of PGI2, was observed to be much higher in the pregnant myometrium than in decidua, amnion, or nonpregnant myometrium. Contrary to the pattern of PGF production, 6-keto PGF1 alpha was lower during labor. The physiological significance of PG production by decidua, amnion, and myometrium in relation to parturition is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Epidermal growth factor-stimulated prostaglandin E2 production in human amnion cells: specificity and nonesterified arachidonic acid dependency.

The production of prostaglandin E2 (PGE2) by human amnion cells in primary monolayer culture was stimulated 2- to 150-fold by mouse epidermal growth factor (mEGF). The effect of mEGF on amnion cell PGE2 production was dependent on the time of treatment and the concentration of mEGF used. The rate of PGE2 production by these cells was maximal between 2 and 4 h of treatment with mEGF; thereafter, the rate of production of PGE2 declined. The stimulation of PGE2 production was maximal at concentrations of mEGF of greater than 5 ng/ml. A number of other growth factors, steroid and protein hormones, and various other test agents were ineffective or only minimally in stimulating PGE2 production by amnion cells. The stimulatory effect of mEGF on PGE2 production in these cells was dependent on the presence of serum in the culture medium; alternatively, mEGF was effective in stimulating PGE2 production by amnion cells in serum-free medium that was supplemented with arachidonic acid bound to albumin. Thus, we conclude that the marked stimulation of PGE2 production by amnion cells treated with mEGF is not due to an action of mEGF to stimulate the release of arachidonic acid from cellular glycerophospholipid storage forms; rather, these data are supportive of the conclusion that mEGF-stimulated PGE2 production is dependent on the presence of nonesterified, i.e., free, arachidonic acid in the medium.

Amnion↗
PubMed1990

Expression and regulation of endothelin precursor mRNA in avascular human amnion.

Posttranslational processing of preproendothelin in endothelial cells gives rise to endothelin, a 21 amino acid polypeptide that is a potent vasoconstrictor. Endothelin production is believed to be mediated principally by transcriptional mechanisms. Previously, preproendothelin mRNA expression has been detected only in vascular endothelial tissue and cells. In this study, we found that preproendothelin mRNA is expressed in an avascular human tissue, namely, amnion, an extraembryonic fetal membrane. Preproendothelin mRNA was not detected in avascular chorion laeve tissue (also an extraembryonic fetal membrane), in the highly vascularized fetal trophoblast, or in maternal uterine tissues. Furthermore, we found that preproendothelin gene expression is retained in human amnion cells maintained in primary monolayer culture. Using the amnion cells in primary monolayer culture to investigate the regulation of preproendothelin mRNA expression, we found that epidermal growth factor (EGF) and interleukin-1 (IL-1) act to stimulate preproendothelin mRNA levels; in addition, the induction of preproendothelin mRNA by either of these agents is enhanced upon simultaneous treatment with cycloheximide. These findings are indicative that preproendothelin gene expression in amnion is regulated positively by EGF and IL-1 and that inhibition of protein synthesis leads to superinduction of preproendothelin mRNA. In human umbilical cord endothelial cells, neither IL-1 nor EGF stimulate preproendothelin mRNA expression but inhibition of protein synthesis does lead to increased levels of preproendothelin mRNA. The amnion, therefore, provides a useful system for expansion of our understanding of the tissue specific expression and regulation of preproendothelin mRNA.

Amnion↗
PubMed1996

Glucocorticoids stimulate prostaglandin H synthase type-2 (PGHS-2) in the fibroblast cells in human amnion cultures.

The human amnion may be an important source of prostaglandins involved in the onset of labour. Glucocorticoids are possible regulators of amnion prostaglandin synthesis and have been shown to stimulate the PGE2 output and prostaglandin H2 synthase (PGHS) activity of human amnion cells maintained in primary monolayer culture. There are two known isoforms of PGHS: the constitutively expressed PGHS-1 and the inducible PGHS-2. Recent studies have shown that the latter isoform is induced by glucocorticoids. The amnion consists of a single layer of epithelial cells beneath which lies a mesenchymal layer containing fibroblasts and it is not known which cell types are responding to glucocorticoids in this manner. In the present study, we demonstrate that although both cell types are present in culture, PGHS-2 protein and mRNA levels increase exclusively within the fibroblasts in response to dexamethasone, while PGHS-1 protein and mRNA levels remain unaffected in both cell types. These results suggest that the stimulation of PGE2 in cultured amnion cells by glucocorticoids is due to an upregulation of PGHS-2 gene transcription in fibroblasts, and that these previously overlooked cells may have important roles to play in the synthesis of prostaglandins involved in labour.

Amnion↗
PubMed1991

Epidermal growth factor and the regulation of amnion prostaglandin biosynthesis.

The production of prostaglandins by amnion is a key factor in the mechanism of human parturition yet the regulation of prostaglandin biosynthesis in amnion is poorly understood. Hence, we have investigated the regulation of epidermal growth factor (EGF) stimulation of prostaglandin biosynthesis in human amnion cells. This stimulatory action is inhibited by cycloheximide or actinomycin D at high concentrations, but enhanced at much lower concentrations of these protein synthesis inhibitors. An amnion-produced prostaglandin inhibitor or immediate early gene action may explain these effects. Pretreatment with phorbol esters (inhibition of protein kinase C activity) reduces basal prostaglandin production and attenuates the stimulatory action of EGF on prostaglandin biosynthesis. Hence, amnion prostaglandin biosynthesis is dependent partly on protein kinase C activity.

Amnion↗
PubMed1994

Actions of interleukin-4 on prostaglandin biosynthesis by human amnion cells.

The effects of interleukin-4 (IL-4) on amnion prostaglandin (PG) production have been determined. Human amnion cells from term placentae were grown to confluence and incubated with IL-4 either alone or with various concentrations of epidermal growth factor (EGF) of ionomycin. PGE2 production was determined using a specific radioimmunoassay. IL-4 alone stimulated PGE2 production in amnion cells in a concentration-related manner. IL-4 significantly enhanced the stimulatory actions of ionomycin and EGF on amnion cell PGE2 production. Ionomycin and IL-4 acted synergistically in their effects on PGE2 production by amnion cells whereas EGF and IL-4 acted more additively in this respect. We suggest that IL-4 production by immune effector cells in gestational tissues may contribute to the mechanisms of labor at term and preterm.

Amnion↗
PubMed2005

Human preterm amnion cells cultured in 3-dimensional collagen I and fibrin matrices for tissue engineering purposes.

OBJECTIVE: In this study, human preterm amnion cells were investigated in 3-dimensional (3D) cell-matrix culture systems in an attempt to design therapeutic strategies for preterm premature rupture of the membranes. STUDY DESIGN: Three-dimensional collagen I and fibrin cell-containing biomatrices were created to mimic the architecture of native amnion. Amnion mesenchymal cells were embedded in 3D matrices, and epithelial cells were placed on top of these matrices. Cell viability and morphology were visualized by DiI-ac-LDL, F-actin, and nuclear staining. Proteolytic activity of matrix metalloproteinases (MMPs) was investigated using gelatine zymography. RESULTS: Preterm amnion epithelial and mesenchymal cells cultured in collagen I and fibrin matrices assume cell morphologies similar to those observed in vivo. Mesenchymal cells were capable of remodelling collagen I, as seen by extensive volume contraction, by 40% at day 1 and 80% at day 5. Matrix contraction was independent of the presence of epithelial cells, and could not be inhibited by GM6001 and/or aprotinin. No contraction was observed in fibrin matrices over 8 days. The migratory response of mesenchymal cells cultured in 3D fibrin matrices supplemented with fibronectin was associated with specific activated MMP-9. CONCLUSION: Three-dimensional fibrin matrices might be useful in amnion cell tissue engineering, including cell-matrix transplantation.

Amnion↗
PubMed1997

In vitro cytokine and prostaglandin production by amnion cells in the presence of bacteria.

OBJECTIVE: Our goal was to evaluate the effect of group B streptococci on cytokine and prostaglandin production by amnion cells in vitro. STUDY DESIGN: Amnion cells from placentas obtained immediately after primary cesarean section were incubated for 48 hours with heat-inactivated group B streptococci at increasing concentrations. 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: Basal cytokine production was not demonstrable for any of the cytokines investigated. Incubation of amnion cells with bacterial antigen led to a significant increase in interleukin-6 and interleukin-8 production, whereas secretion of interleukin-1 beta and tumor necrosis factor-alpha was not enhanced. In contrast to cytokines, basal prostaglandin E2 production was measurable but failed to increase after addition of antigen. CONCLUSION: Amnion cells can be stimulated to secrete interleukin-6 and interleukin-8 in response to streptococcal antigen. However, this rise in cytokines does not induce an increase in prostaglandin E2. This may be explained by the lack of interleukin-1 and tumor necrosis factor-alpha production, two cytokines that have been shown to activate prostaglandin E2 secretion by amnion cells.

Amnion↗
PubMed1998

Immunohistochemical localization of inducible nitric oxide synthase on human fetal amnion in intra-amniotic infection.

OBJECTIVES: Amniotic fluid levels of nitric oxide metabolites are significantly elevated in intra-amniotic infection. We hypothesized that fetal amnion is a possible site for the production of nitric oxide. Because inducible nitric oxide synthase is the key enzyme responsible for the generation of nitric oxide in patients with intra-amniotic infection, we used immunohistochemistry to localize it on human fetal amnion. STUDY DESIGN: Human fetal amnions were obtained from patients with and without intra-amniotic infection (n = 5, respectively). Intra-amniotic infection was diagnosed by positive amniotic fluid cultures and placental pathologic features. Human fetal amniotic membranes were processed into tissue blocks and embedded in paraffin. A rabbit polyclonal antibody against human inducible nitric oxide synthase was used as the primary antibody, followed by avidin-biotin immunoperoxidase localization. Normal rabbit serum was used as a negative control and ovarian carcinoma cells were used as the positive control. RESULTS: Anti-inducible nitric oxide synthase labeling of human fetal amniotic membranes in patients with intra-amniotic infection showed positive immunostaining of epithelial cells, specifically in the cytoplasm of the perinuclear area. In contrast, no anti-inducible nitric oxide synthase immunostaining on human fetal amniotic membranes could be identified in patients without intra-amniotic infection. CONCLUSIONS: Our data provide important evidence that inducible nitric oxide synthase can be induced on human fetal amnion in intra-amniotic infection. These findings strongly support our hypothesis that human fetal amnion may be a possible site for the synthesis of nitric oxide after inducible nitric oxide synthase is induced in response to infectious products in intra-amniotic infection.

Amnion↗