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PubMed1991

A hybrid form of alkaline phosphatase produced in FL-amnion cells.

FL-amnion cells have mainly two alkaline phosphatase (AP) isozymes, of which the faster migrating one (FL-APF) on 5% polyacrylamide gel electrophoresis has proved to be identical to the Kasahara isozyme, a tumor-associated AP of intestinal type. But the other slower migrating one (FL-APs) remains to be characterized. Immunological and enzymic examination of purified FL-APs revealed that it is a hybrid form of AP consisting of one subunit with a molecular weight of 66,200 coming from the same subunit as that of FL-APF and another one with a molecular weight of 58,000 from placental AP subunit with modified glycosylation.

Alkaline Phosphatase↗
PubMed1962

Sedimentation and autoradiographic analyses of rapidly labeled ribonucleic acids in human amnion cells.

When human amnion cells were exposed to radioactive cytidine for 0.002 or 0.017 of one generation time, the alcohol-insoluble label in the RNA preparations from these cells was distributed between a rather homogeneous component of 4 to 8S and a fast mixture of 34S, 30S, 25S, 20S, and 15S. Evidence has been presented that these sedimenting components are RNA. More than 73 per cent of the label in the fast mixture from the cells labelled for 0.017 of one generation time was derived from the nuclei. The label in nucleotides after 0.017 of one generation time equaled 1.4 times that in RNA. Thus, the previous autoradiographic evidence for the nuclear origin of late cytoplasmic label is weak. The distribution of label among the various sedimenting components, as well as that between two pyrimidine nucleotide constitutents of 34S, 30S, 25S, and 15S components, changed when the length of exposure to radioactive cytidine was increased from 0.002 to 0.017 of one generation time. This result excluded the possibility that the population of the RNA labeled after 0.002 of one generation time was identical with that labeled later. This fact must be included in formulation of hypotheses for the function of rapidly labeled RNA's.

Amnion↗
PubMed1995

Activation of phospholipase D in cultured human amnion cells.

The regulation of phospholipase D (PLD) activity in the human amniotic membrane was examined using primary cultures of amnion cells. Cultured amnion cells were labelled with [3H]oleic acid, and PLD activity was determined as the amount of [3H]phosphatidylethanol (PEt) produced during incubation in the presence of 0.1% ethanol. PLD activity in cultured amnion cells was activated by addition of arginine vasopressin and oxytocin. PLD activity was also stimulated by treatment was arachidonic acid, the product of phospholipase A2 (PLA2), and phospholipase C (PLC). These results indicate that PLD in amnion cells is activated by substances present in amniotic fluid, and that cross-talk between phospholipases A2, C and D may occur in amnion cells.

Amnion↗
PubMed1993

Expression of functional insulin-like growth factor-I receptors by human amnion cells.

OBJECTIVES: The purpose of the study was to investigate whether amnion cells contain functional insulin-like growth factor-I receptors. STUDY DESIGN: To test whether human amnion cells contain insulin-like growth factor-I receptors, radioligand binding studies, affinity cross-linking studies, and Northern blot analysis were conducted in primary amnion cells and in an immortal amnion cell line (WISH). To test whether the insulin-like growth factor-I receptors on amnion cells are functional, cytochalasin B-inhibitable 2-deoxyglucose uptake was measured after stimulating the cells with insulin-like growth factor-I. RESULTS: Radioligand binding studies demonstrated that primary amnion cells and WISH cells contained a single class of high-affinity receptors with an apparent dissociation constant of 0.18 +/- 0.04 nmol/L and a receptor concentration of 79 +/- 26.2 fmol/mg protein and dissociation constant of 0.44 +/- 0.03 nmol/L and a receptor concentration of 33.3 +/- 6.45 fmol per 106 cells, respectively. Affinity cross-linking studies revealed two major insulin-like growth factor-I binding sites, 135 and 270 kd. Both primary amnion cells and WISH cells exhibited cytochalasin B-inhibitable tritiated 2-deoxyglucose uptake in response to insulin-like growth factor-I treatment. Finally, treatment of WISH cells caused tyrosine phosphorylation of three proteins (molecular weight, 116, 95.4, and 83.5 kd) was observed by Western blotting with antiphosphotyrosine antibodies. CONCLUSION: These results provide the first evidence that human amnion epithelial cells contain functional high-affinity insulin-like growth factor-I receptors that mediate glucose transport.

Amnion↗
PubMed1984

Characterization of prostaglandin formation by human amnion cells in monolayer culture.

In the present investigation, we found that among the prostanoids that human amnion cells, which are maintained in monolayer culture, secrete into the culture medium, prostaglandin E2 is by far the predominant one. In the presence of inhibitors of prostaglandin synthase, the production of prostaglandin E2 by these cells is abolished. Amnion cells maintained in the presence of fetal calf serum produce greater quantities of prostaglandin E2 than do cells maintained in serumless medium. In the amnion cells, there is little or no metabolism of prostaglandin E2; this also is true of amnion tissue. The unique characteristics of prostaglandin biosynthesis and metabolism by human amnion cells in monolayer culture are identical with those of human amnion tissue. Hence, we suggest that amnion cells in culture constitute an excellent model for investigations of the regulation of prostaglandin E2 biosynthesis in this tissue.

Amnion↗
PubMed2006

[Human amnion cells express the phenotypes of neural cells and adipocytes in vitro].

OBJECTIVE: To search for culture conditions in which the cells from human amnion could diferentiate into neural cells and hence to explore a new cell source for neural transplantaion. METHODS: Amnion cells from human were cultured with tissue piece method, passaged by trypsin digestion and identified with immunocytochemistry. RESULTS: Amnion cells migrated from explants and primary culture was established; they could multiply and expand steadily in a short time, and they could be passaged by trypsin digestion. When cultured in serum-free neural stem cell media, these cells could form the same spheroid shape as the neurospheres of neural stem cells. They could express alpha smooth muscle actin and differentiate into smooth muscle cells spontaneously, and could express nestin and vimentin, the markers for neural progenitors. Moreover, they could he stained by anti-beta III-tubulin, anti-neurofilament 200 and anti-NSE; the majorities could he stained by antityrosine hydroxylase, the marker for dopaminergic neurons. Lower than 0.1% of the total cells were stained by GFAP, indicating the existence of astrocytes. The amnion cells could also differentiate into adipocytes under specific induction. CONCLUSION: Amnion cells could differentiate into adipocytes and smooth muscle cells; they could express the protein for neural cells; thus may represent an alternative stem cell source for CNS cell transplantation.

Adipocytes↗
PubMed1961

Pathogenicity for suckling mice of Coxsackie viruses adapted to human amnion cells.

Continuous passages in primary human amnion cell cultures of Coxsackie prototype viruses A-9, A-10, A-11, A-13, A-14, A-15, A-18, B-1, B-2, B-4, and B-5 increased the titers, hastened and enhanced cytopathic effect, and in varying degrees caused loss of virulence for newborn mice. Only B-3 behaved differently in that neither adaptation to cells in vitro nor attenuation with respect to the original animal host could be observed. Types A-15, B-1, B-2, and B-5 slowly regained virulence when passed in mice after high concentration passages in amnion cells whereas all other viruses reverted to their original virulence after only 1 or 2 passages in the animal host. When these strains, however, were purified by cloning procedures, they too showed markedly increased stability. In all stages of attenuation, viruses multiplied extensively in vivo as could be shown by titration in amnion cell cultures. It is suggested that a genetic mechanism is operative leading to virus populations in which the majority of the particles is qualitatively changed.

Amnion↗
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↗
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↗
PubMed1994

Transforming growth factor-beta stimulates, and glucocorticoids and epidermal growth factor inhibit brain natriuretic peptide secretion from cultured human amnion cells.

We previously reported the massive secretion of brain natriuretic peptide (BNP) from human amnion cells and suggested the possible role of BNP in the maintenance of human pregnancy. In this study, to elucidate the regulatory mechanism of BNP secretion from amnion cells, we measured the BNP level in the culture medium of amnion cells by RIA after incubation in the presence of various substances. Among the agents examined, cortisol (1 x 10(-7) to 1 x 10(-6) mol/L), dexamethasone (1 x 10(-8) to 1 x 10(-6) mol/L), and epidermal growth factor (EGF; 2 x 10(-11) to 2 x 10(-8) mol/L) inhibited BNP secretion from the cultured amnion cells in a dose-dependent manner. By contrast, transforming growth factor-beta (TGF beta; 4 x 10(-11) to 4 x 10(-9) mol/L) caused a 3- to 5-fold increase in BNP secretion. TGF beta-augmented BNP secretion was abolished by the addition of cortisol or EGF to the culture medium. Moreover, in this study, we revealed the presence of bioactive TGF beta in human amniotic fluid (approximately 4 x 10(-10) mol/L). The present finding of tight regulation of BNP secretion from amnion cells by cortisol, EGF and TGF beta, all at the concentrations physiologically present in human amniotic fluid, implies a physiological role of BNP secretion from amnion cells in the pregnant uterus.

Amnion↗
PubMed1991

Renin increases human amnion cell prostaglandin E2 biosynthesis.

Chorionic cells are known to produce several protein hormones; among them is prorenin/renin, whose function is unknown at this time. Amnion is contiguous with chorion and plays a part in the mechanism(s) of parturition through increased prostaglandin (PG) production. The purpose of the present study was to determine whether renin has any action on amnion cell PGE2 biosynthesis. Amnion cells in primary monolayer culture were incubated for 16 h with increasing concentrations of renin. Renin induced a concentration-dependent increase in amnion cell PGE2 production (e.g. in picograms of PGE2 per microgram protein/16 h; mean +/- SEM; n = 4; control, 3.01 +/- 0.15; 0.0001 U/mL renin, 9.66 +/- 2.0; 0.001 U/mL renin, 10.36 +/- 1.91; 0.01 U/mL renin, 10.3 +/- 3.36; 0.1 U/mL renin, 13.82 +/- 2.1). Significant stimulation of amnion cell PGE2 by renin is not observed until 2 h of incubation; stimulation continues a further 6 h, with little change in the following 8 h. We tested the possibility that renin's stimulatory effects were due to angiotensin-I (AI) and angiotensin-II (AII) formation by testing the effects of AI and AII directly and that of renin in the presence of saralasin, a potent antagonist of AII action. Saralasin did not inhibit the effect of renin, nor was AI or AII alone (10(-10)-10(-6) M) stimulatory. Thus, we believe that chorionic renin may have a novel role in the regulation of amnion cell PGE2 production that is independent of angiotensin formation.

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↗
PubMed1993

Epidermal growth factor and transforming growth factor-alpha enhance the interleukin-1- and tumor necrosis factor-stimulated prostaglandin E2 production and the interleukin-1 specific binding on amnion cells.

Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. During labor occurring in the setting of infection, several of these cytokines may be simultaneously present in amniotic fluid. The aim of the present study was to examine whether these cytokines modify each others' effects on amnion cell PGE2 production. Amnion cells in monolayer culture were treated with IL-1, TNF, EGF, TGF-alpha, TGF-beta 1, their combination, or vehicle. The PGE2 production and the specific binding of radiolabeled IL-1 beta on the cells were measured. IL-1 or TNF in combination with EGF or TGF-alpha stimulated synergistically the production of PGE2 by amnion cells. TGF-beta 1 did not modify the PGE2-stimulatory effect of EGF/TGF-alpha. Untreated amnion cells expressed 1030 +/- 100 IL-1 beta receptors per cell with a binding affinity of 1.40 +/- 0.26 nM. Treatment with TGF-alpha increased the number of receptors to 3940 +/- 260 per cell with no change in binding affinity. The potentiation of the PGE2-stimulatory effect of IL-1 by TGF-alpha may be related to its ability to induce IL-1 receptors on amnion cells. The synergistic effects of cytokines on amnion cell PGE2 production may promote labor.

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↗
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↗
PubMed1989

Effect of lipid and protein fractions from fetal pulmonary surfactant on prostaglandin E production by a human amnion cell line.

Discs of amnion and choriodecidua prepared from women delivered at term were incubated with and without surfactant prepared from human amniotic fluid and the output of prostaglandin E (PGE) was estimated by radioimmunoassay. Surfactant stimulated the release of PGE in both tissues. The stimulatory effect was characterized further using cultured human amnion cells. The effect was dose- and time-dependent and required for full expression both protein and lipid components of surfactant. Arachidonate constituted about 3.5% of the fatty acids of fetal surfactant phospholipids. These findings suggest that surfactant is an important source of arachidonate for intrauterine PG synthesis.

Amnion↗