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PubMed1992

Transforming growth factor-beta opposes the stimulatory effects of interleukin-1 and tumor necrosis factor on amnion cell prostaglandin E2 production: implication for preterm labor.

OBJECTIVE: In preterm labor increased concentrations of interleukin-1 and tumor necrosis factor are present in amniotic fluid. These cytokines may promote labor by stimulating the production of prostaglandins by intrauterine tissues. In many biologic processes, transforming growth factor-beta modifies the actions of cytokines. We studied the effect of transforming growth factor-beta on the cytokine-induced prostaglandin E2 production by amnion cells. STUDY DESIGN: Human amnion cells in monolayer culture were treated with interleukin-1, tumor necrosis factor, or vehicle in the presence or absence of transforming growth factor-beta. The prostaglandin E2 production was measured. RESULTS: Transforming growth factor-beta decreased the interleukin-1- or tumor necrosis factor-induced prostaglandin E2 production by 70% to 80% and the basal prostaglandin E2 synthesis by 27%. The synergistic stimulation of prostaglandin E2 production by the combination of interleukin-1 with tumor necrosis factor was inhibited by 80% in cells treated with transforming growth factor-beta. Transforming growth factor-beta 1, -beta 2, and -beta 1,2 were equipotent. CONCLUSION: Transforming growth factor-beta suppresses the cytokine-induced prostaglandin E2 production by amnion cells and may be an important factor in maintaining pregnancy in the face of labor-promoting cytokines.

Amnion↗
PubMed1993

Ritodrine: a beta-adrenergic receptor antagonist in human amnion.

OBJECTIVE: Human amnion is important in the initiation of labor. Ritodrine, when administered as a tocolytic, is found unchanged in amniotic fluid. We characterized effects of ritodrine binding to beta-adrenergic receptors in amnion and amniocytes. STUDY DESIGN: Iodine 125-iodopindolol, beta-adrenergic receptor agonists, and beta-adrenergic receptor antagonists were used to describe binding characteristics. Experiments were designed with and without isoproterenol and ritodrine to study intracellular cyclic adenosine 3'5'-monophosphate and prostaglandin E2 release. RESULTS: Scatchard analysis revealed a single class of saturable binding sites, with maximum binding capacity of 70.0 +/- 17.2 fmol/mg protein (n = 12) and with high-affinity dissociation constant of 458.9 +/- 72.1 pmol/L. Agonists and antagonists competed for the 125I-iodopindolol binding site consistent with a beta 2-adrenergic receptor. Hill coefficients were 0.6 to 0.8 for agonist competition and 1.0 for antagonist competition and ritodrine. Stimulation with isoproterenol resulted in dose-dependent increases in cyclic adenosine 3'5'-monophosphate and prostaglandin E2. Ritodrine failed to stimulate cyclic adenosine 3'5'-monophosphate and inhibited isoproterenol-stimulated cyclic adenosine 3'5'-monophosphate and prostaglandin E2 production. CONCLUSION: In human amnion binding of ritodrine to beta 2-adrenergic receptors and lack of ritodrine-mediated postreceptor effects are characteristic of a beta 2-adrenergic antagonist.

Amnion↗
PubMed1988

Arachidonic acid incorporation into lipids of term human amnion.

There were no differences in the rate or amount of (1-14C)-labeled arachidonic acid incorporated into triacylglycerides, diacylglycerides, or any phospholipid species of freshly dispersed term human amnion cells obtained before or after labor. Both phosphatidylcholine and phosphatidylethanolamine incorporated 14C-arachidonic acid in proportion to their molar percent of total amnion phospholipids, but phosphatidylinositol incorporated three times as much 14C-arachidonic acid, suggesting either a rapid turnover in this specific phospholipid pool or a greater specificity for the transfer of arachidonoyl-coenzyme A to lysophosphatidylinositol. No or little competition of 14C-arachidonic acid incorporation into triacylglycerides or phospholipids occurred with palmitic acid, linoleic acid, or gamma-linolenic acid. However, dihomo-gamma-linolenic acid, eicosapentaenoic acid, and unlabeled arachidonic acid were effective inhibitors. We conclude that the term amnion has high acyl transferase activity, that no change in the basal activity of this enzyme occurs with the onset of labor, and that a specific acyl transferase exists for 20-carbon polyunsaturated fatty acids.

Amnion↗
PubMed1998

Regulation of prostaglandin H2 synthase-2 expression in primary human amnion cells by tyrosine kinase dependent mechanisms.

Prostaglandin H2 synthase (PGHS)-1 and PGHS-2 expression was examined in primary cultures of human amnion cells, an in vitro model of amnion tissue. Epidermal growth factor (EGF), the protein kinase C (PKC) activating phorbol ester TPA, and the protein phosphatase inhibitor, okadaic acid (OA), stimulated PGHS activity and the level of PGHS-2 mRNA, but did not affect the level of PGHS-1 mRNA. In situ hybridization suggested that the same population of cells responded to EGF, TPA and OA. Okadaic acid promoted PGHS activity independently of PKC. EGF stimulated the activity of extracellular signal-regulated protein kinase (Erk) and N-terminal c-Jun kinase (Jnk). OA increased Jnk activity but had no effect on Erk activity, while TPA had no influence on either Erk or Jnk activity. PD098059, a selective inhibitor of the Erk-activating kinase MEK, blocked the stimulation of PGHS expression by EGF, but did not decrease stimulation in response to OA. Herbimycin A, a tyrosine kinase inhibitor, suppressed the stimulation of PGHS activity and PGHS-2 mRNA abundance by all three stimulants, and blocked signalling via the Erk and Jnk mitogen-activated protein kinase pathways. Thus, growth factor stimulation, PKC activation and protein phosphatase inhibition induced the expression of PGHS-2 in primary amnion cells by distinct regulatory mechanisms involving tyrosine kinase(s). Tyrosine kinase inhibitors may constitute a new category of PGHS-2 inhibitors that act by blocking the expression of the enzyme.

Amnion↗
PubMed2001

Progesterone receptor isoform A inhibits isoform B-mediated transactivation in human amnion.

Human amnion cells were transfected with progesterone receptor A and/or B, and the progesterone-dependent reporter construct, mouse mammary tumor virus promoter (MMTV), linked to a luciferase gene. In progesterone receptor B-expressing amnion that had been cultured before the onset of labour, treatment with progesterone resulted in an eightfold increase of the reporter activity, whereas in laboured cells, no such increase was seen. In contrast, progesterone receptor A was a weak activator of transcription in laboured and non-laboured amniocytes. When the isoforms A and B of the progesterone receptor were co-transfected, progesterone receptor A exhibited a marked inhibitory effect on progesterone receptor B-mediated transcription. These results show that progesterone receptors A and B function differentially, and progesterone receptor A is a transdominant repressor of progesterone receptor B-mediated transcription in human term amnion.

Amnion↗
PubMed1980

Treatment of chronic ulceration of the legs with human amnion.

Chronic leg ulcers in fifteen patients were prepared for autografting with a dressing of cultured human amnion. In thirteen vascular responses filled the ulcer beds with granulation tissue. Four patients initially received more traditional therapy and their lesions altered little in gross appearance and were not regarded clinically to have produced a granulation-tissue response. Fourteen patients received autografts after 5 days of amnion application and eight of these grafts have remained intact for 2-10 months. The appearance of healthy granulation tissue after amnion application was associated with successful autografting.

Adult↗
PubMed1980

Human amnion as an adjunct in wound healing.

Biopsy specimens from the beds of leg ulcers of fifteen patients were obtained before and after the application for 5 days of cultured human amnion. After amnion application there was considerable granulation tissue in the ulcer bed and microscopical evidence of thinned connective tissues, vessel development, more compact resolution of vascular basement membranes, and many more factor VIII granules within endothelial cells. These findings suggest the presence of angiogenic factors in human amnion and this could explain the hitherto unexplained success of amniotic membranes in surgical practice.

Amnion↗
PubMedDate not supplied

Regulation of activin-A production by human amnion, decidua and placenta in vitro by pro-inflammatory cytokines.

Activin-betaA subunits are expressed by the human placenta and extraplacental membranes at term and preterm. The regulation of activin-A production by these tissues has not been characterized to date, however. To determine the effects on activin-A production of pro-inflammatory cytokines, amnion, decidual and placental cells were isolated by enzyme dispersion and treated in primary culture with interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha). Activin-A production (determined by ELISA) by amnion, decidual and placental cultures was 1.2 +/-0.27, 31.1+/-9.9, and 50.7+/-28.5 pg/microg protein/16 h, respectively (mean+/-SEM; n=5-7 experiments). Both IL-1beta and TNF-alpha stimulated activin-A production in a concentration-dependent fashion in all cultures; maximal stimulation was achieved at 0.25-1.0 ng/ml IL-1beta and 25-50 ng/ml TNF-alpha, respectively. In amnion, decidual and placental cultures IL-1beta stimulated activin-A production to 747+/-274, 190+/-11, and 254+/-60.2 per cent of controls, while TNF-alpha stimulated production to 312+/-81.5, 194+/-22.5, and 193+/-12.5 per cent, respectively (mean+/-SEM; n=5; P<0.05 by ANOVA). These studies show for the first time that pro-inflammatory cytokines are potent stimulators of activin-A production by intrauterine tissues. This may provide an explanation for the elevated concentrations of activin-A measured in the sera of some women in preterm labour.

Activins↗
PubMed2001

Effect of ceramide analogs on interleukin-1alpha-induced production of prostaglandin E2 by amnion-derived (WISH) cells.

BACKGROUND: Prostaglandin E2 (PGE2) is reportedly synthesized in the amnion, and its levels are increased during labor. Our objective was to measure the level of PGE2 induced by interleukin (IL)-1alpha following treatment with ceramide analogs in amnion-derived cells. METHODS: Amnion-derived (WISH) cells were cultured and stimulated by IL-1alpha, IL-1 receptor antagonist (ra), C2-ceramide and C6-ceramide. The levels of PGE2 in the media were measured by ELISA. The induction of prostaglandin H synthase (PGHS)-2 mRNA was detected by reverse transcription and polymerase chain reaction (RT-PCR). RESULTS: Following stimulation with IL-1alpha, the production of PGE2 could not be detected until incubation had continued for 2 h, but this production appeared to continue after 4 h of incubation. The production of PGE2 was significantly increased by IL-1alpha, and was suppressed by IL-1 ra, in a dose-dependent manner. PGE2 production was significantly increased by IL-1alpha and C2-ceramide as compared with IL-1alpha alone. However, PGE2 production was not significantly increased by IL-1alpha and C6-ceramide as compared with IL-1alpha alone. PGHS-2 mRNA were induced by treatment with IL-1alpha, and were strongly induced by treatment with IL-1alpha and C2-ceramide by RT-PCR. CONCLUSIONS: Results suggest that IL-1alpha induce the PGHS-2 mRNA and stimulate the production of PGE2 by a mechanism that involves the sphingomyelin-ceramide system. Ceramide may be important in increasing the production of PGE2 during parturition.

Amnion↗
PubMed1999

Cytokines regulate prostaglandin H synthase-1 transcription in human amnion-derived cells.

We have isolated the prostaglandin H synthase-1 (PGHS-1) promoter from the human amnion cell line WISH by long template PCR. The fragment was 1124 base pairs in length and shared a 96% sequence identity with the sequence in GenBank. The putative transcription start site is located 18 bp upstream of the start codon. The sequence is TATA-less, but contains multiple Sp-1 sites and a GC box at -132. The fragment was subcloned into the promoterless reporter construct pBLCAT3 to produce the promoter reporter construct pPGHS1CAT. pPGHS1CAT expression in amnion-derived AV3 cells was inhibited by the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin 1-beta (IL-1beta). PGHS-1 mRNA levels however, were unchanged over a 16-h time course with either treatment. These results suggest that PGHS-1 transcription is regulated in a negative manner by cytokines in human amnion-derived cells.

Amnion↗
PubMed1991

Adsorption of fetal surfactant protein SP-B on the human amnion at term and on amniocytes incubated with fetal surfactant in vitro.

Fetal surfactant stimulates the synthesis of prostaglandins by slices of human amnion at term and by a human amnion cell line, and these effects are partly dependent upon surfactant apoproteins. In this paper, methods are described for the purification of surfactant from human amniotic fluid and from post-mortem human lung. A procedure is described for the purification of surfactant protein SP-B from human amniotic fluid, and the sequence of 20 amino acids at the N-terminal has been determined. A monoclonal antibody generated against human lung surfactant has been shown to react with SP-B from amniotic-fluid surfactant, and the presence of SP-B on the surface of the amnion at term has been demonstrated by immunohistochemical methods. It has also been shown that SP-B from surfactant is present on the surface of amniocytes incubated with surfactant in vitro.

Adsorption↗
PubMed1997

Hypotonic stress increases cyclooxygenase-2 expression and prostaglandin release from amnion-derived WISH cells.

This report examines the effect of cell volume expansion on cyclooxygenase-2 (COX-2) mRNA expression, COX-2 protein expression, and prostaglandin E2 release from human amnion-derived WISH cells. Earle's balanced salts solution (EBSS) with limited NaCl concentration was utilized as the induction medium. COX-2 mRNA was elevated 6-fold in cells incubated for 1 h in hypotonic EBSS. COX-2 mRNA expression was not increased when raffinose or sucrose were used to reconstitute low NaCl. Actinomycin D blocked COX-2 mRNA increase by hypotonic stress, while cycloheximide enhanced COX-2 mRNA expression. COX-2 mRNA and protein concentrations increased as a function of decreasing media osmolarity and incubation time in hypotonic EBSS. Hypotonic EBSS induced a 3-fold increase in prostaglandin E2 release. WISH cells transiently transfected with a luciferase expression vector driven by the human COX-2 promoter for the COX-2 gene show a 3-fold increase in luciferase activity when incubated in hypotonic EBSS. COX-2 mRNA levels in primary human amnion cells were also increased by hypotonic stress. This study suggests that amnion cell COX-2 gene expression is regulated by cell volume expansion and/or increased plasma membrane tension.

Amnion↗
PubMed1998

Involvement of phosphatidate phosphohydrolase in arachidonic acid mobilization in human amnionic WISH cells.

Prostaglandins are known to play a central role in the initiation of labor in humans, and amnionic cells constitute a major source of these compounds. Prostaglandin synthesis and release by amnion cells in response to hormones and ligands takes place after a characteristic 4-5 h lag. However, we report herein that free arachidonic acid (AA), the metabolic precursor of prostaglandins, can be induced at much shorter times (1 h) in human amnionic WISH cells by phorbol 12-myristate 13-acetate (PMA) through activation of protein kinase Calpha (PKCalpha). WISH cells were found to possess both cytosolic group IV phospholipase A2 (cPLA2) and Group VI Ca2+-independent phospholipase A2 (iPLA2). Of these, the cPLA2 was found to be the likely mediator of AA mobilization in PMA-activated WISH cells. PMA also activates phospholipase D (PLD) in these cells and ethanol, a compound that inhibits PLD-mediated phosphatidic acid (PA) formation, blocked AA release. Moreover, prevention of PA dephosphorylation by the PA phosphohydrolase inhibitors propranolol and bromoenol lactone, resulted in inhibition of AA release by PMA-treated WISH cells. Collectively, these data suggest that activation of cPLA2 and attendant AA release by phorbol esters in WISH cells requires prior generation of DAG by phosphatidate phosphohydrolase.

Amnion↗
PubMed1996

Human amnion contains a novel laminin variant, laminin 7, which like laminin 6, covalently associates with laminin 5 to promote stable epithelial-stromal attachment.

Stable attachment of external epithelia to the basement membrane and underlying stroma is mediated by transmembrane proteins such as the integrin alpha6beta4 and bullous pemphigoid antigen 2 within the hemidesmosomes along the basolateral surface of the epithelial cell and their ligands that include a specialized subfamily of laminins. The laminin 5 molecule (previously termed kalinin/nicein/epiligrin) is a member of this epithelial-specific subfamily. Laminin 5 chains are not only considerably truncated within domains III-VI, but are also extensively proteolytically processed in vitro and in vivo. As a result, the domains expected to be required for the association of laminins with other basement membrane components are lacking in the mature laminin 5 molecule. Therefore, the tight binding of laminin 5 to the basement membrane may occur by a unique mechanism. To examine laminin 5 in tissue, we chose human amnion as the source, because of its availability and the similarity of the amniotic epithelial basement membrane with that of skin. We isolated the laminin 5 contained within the basement membrane of human amnion. In addition to monomeric laminin 5, we find that much of the laminin 5 isolated is covalently adducted with laminin 6 (alpha3beta1gamma1) and a novel laminin isotype we have termed laminin 7 (alpha3beta2gamma1). We propose that the association between laminin 5 and laminins 6 and 7 is a mechanism used in amnion to allow stable association of laminin 5 with the basement membrane. The beta2 chain is seen at the human amniotic epithelial-stromal interface and at the dermal-epidermal junction of fetal and adult bovine skin by immunofluorescence, but is not present, or only weakly present, in neonatal human skin.

Adult↗
PubMed1958

A comparison of the growth of selected mycobacteria in HeLa, monkey kidney, and human amnion cells in tissue culture.

HeLa, monkey kidney, and human amnion cells in tissue cultures were compared as sites for the multiplication of strains of tubercle bacilli or original and reduced pathogenicity, and for several other species of mycobacteria capable of causing disease in humans. The arrangement of the pathogenic species inorder of their growth rates in HeLa cells was Mycobacterium fortuitum, Mycobacterium balnei, and the "yellow bacillus," followed closely by the tubercle bacillus. This order was also correct for these species in monkey kidney and human amnion cells, and is the same as that seen in bacteriological media. The arrangement of the strains of tubercle bacilli in order of their growth rates in all three types of cells was: H37Rv, then R1Rv, and lastly H37Ra, which multiplied about as slowly as BCG. An INH-resistant strain grew about as rapidly as H37Rv. Growth of the pathogenic species occurred at about the same rates in HeLa and monkey kidney cells, but was distinctly slower in human amnion cells, which are less active metabolically. Irradiation of the cells in doses up to 5000 r did not affect the subsequent growth of mycobacteria in them. Preliminary experiments with human leprosy bacilli indicate that they can be introduced into these cells in high numbers and that the bacilli then persist for the life of the cells.

Amnion↗
PubMed1998

Tumor necrosis factor-alpha upregulates the prostaglandin E2 EP1 receptor subtype and the cyclooxygenase-2 isoform in cultured amnion WISH cells.

Recent studies have demonstrated a strong correlation between infection and preterm labor. Preterm delivery is also associated with high levels of cytokines and prostaglandins in amniotic fluid. The purpose of this study was to investigate the effect of tumor necrosis factor-alpha (TNF-alpha) on the levels of cyclooxygenase, prostaglandin E2 production (PGE2), and expression of the PGE2 receptor subtype EP1 in amnion WISH cell culture. Amnion WISH cell cultures were incubated in increasing concentrations of TNF-alpha (0-50 ng/ml). Changes in cyclooxygenase and EP1 receptor proteins were evaluated by Western blot analysis. Changes in EP1 mRNA were evaluated by Northern blot, and culture fluid concentrations of PGE2 were estimated by enzyme immunoassay (EIA). EP1 protein (p<0.01), EP1 mRNA (p<0.05), cyclooxygenase-2 (COX-2) protein (p<0.001), and PGE2 concentrations (p<0.01) all increased with increasing concentrations of TNF-alpha. Changes in COX-1 protein were not observed following TNF-alpha-incubation. The results suggest that TNF-alpha may play a role in infection-induced preterm labor by its pleiotropic ability to simultaneously stimulate COX-2 activity, PGE2 concentrations, and PGE2 EP1 receptor levels in human amnion.

Amnion↗
PubMed1979

Infection of untreated primary human amnion monolayers with Chlamydia trachomatis.

For development of a laboratory model for chlamydial infection of the human genital tract, untreated primary human epithelial cell monolayers, prepared from each of four placentas, were infected with a stock strain of Chlamydia trachomatis isolated from the nasopharynx of an infant with pneumonia. Infectivity titrations were performed with use of standard procedures of chlamydial inoculation, and inclusions grown in amnion cell monolayers and in McCoy cells were measured versus infectious units inoculated. By linear regression analysis, untreated human amnion cells (y = 0.948x + 4.63, r = 0.9255) were as susceptible as McCoy cells treated with diethylaminoethyl dextran and 5-iodo-2-deoxyuridine (y = 1.104x + 5.35, r = 0.9804). Human amnion may prove a valuable model for study of human chlamydial infection and may have important implications for investigation of clinical disease.

Amnion↗
PubMed1989

Mechanisms of cellular invasiveness: a comparison of amnion invasion in vitro and metastatic behavior in vivo.

We employed a sensitive in vitro amnion invasion assay to examine the relationship of the invasive ability of numerous mouse and human tumor cell lines and their variants to their ability to spontaneously or artificially metastasize; we also studied possible enzymatic activities involved in the in vitro invasion process. In vitro invasive ability of tumor cells was strongly correlated with spontaneous metastatic ability from the subcutaneous site, regardless of the ability of tumor cells to form artificial metastases when introduced intravenously. However, normal nontumorigenic human trophoblast cells were also highly invasive. Various collagenase inhibitors totally abrogated amnion penetration by all invasive cells; various inhibitors of plasmin, plasminogen, and plasminogen activators prevented invasion in most, but not all, cases. Thus, amnion penetration provides a rigorous test for tumor cell invasiveness required for spontaneous metastasis in vivo, and invasiveness is strongly dependent on metalloproteinase activity, which usually follows plasmin activation.

Amnion↗