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PubMed1983

Calcium and phosphate fluxes across the fetal membranes of the guinea pig: in vitro measurement.

Bidirectional calcium (45Ca) and phosphate (32P) fluxes across the amnion and visceral yolk sac of the guinea pig were measured in vitro in modified Ussing chambers. The net flux of these ions across both fetal membranes was in the maternal-to-fetal direction. The net flux of 45Ca and 32P across the yolk sac was significantly greater than that across the amnion. This difference was due to a greater maternal-to-fetal flux across the yolk sac. In addition, net 32P flux was greater than net 45Ca flux across the yolk sac, while in the amnion, there was no significant difference in the net flux of the two ions. It is suggested that the fetal membranes, especially the visceral yolk sac, contribute significantly to fetal acquisition of calcium and phosphate in mammals possessing a functional yolk sac placenta.

Amnion↗

PubMed1989

Local stimulation of prostaglandin production by corticotropin-releasing hormone in human fetal membranes and placenta.

Corticotropin-releasing hormone is produced by the human placenta and fetal membranes, but its physiological significance is not established. We examined the possibility that CRH might affect prostaglandin output by these intra-uterine tissues. Primary cultures of amnion, chorion, decidua and placenta were established from tissue obtained from women at term elective cesarean section were maintained in the presence of increasing concentrations of synthetic hCRH. PG output at 48h was measured by radioimmunoassay. hCRH stimulated PGE2 output by amnion, chorion and placenta, but not by decidual tissue. PGF2 alpha output was stimulated in amnion, decidua and placenta but not chorion, whereas output of 13, 14-dihydro-15-keto PGF2 alpha was stimulated in all four tissues. We conclude that hCRH stimulates prostaglandin output by human placenta, decidua and the fetal membranes, raising the possibility of paracrine or autocrine interactions between CRH and prostaglandins in vivo.

Amnion↗

PubMed1983

Specific glucocorticoid binding in human uterine tissues, placenta and fetal membranes.

The binding of [3H]dexamethasone to cytosol fractions of human myometrium, endometrium, decidua, chorion, amnion and placenta has been studied. All tissues examined contained high affinity, low capacity binding sites with high specificity for glucocorticoids. Maximum specific binding of [3H]dexamethasone was reached after about 10 h at 0-4 degrees C and remained stable for at least the next 12 h. Sucrose density gradient analysis showed that the binding macromolecules sedimented at 7.9 S in hypotonic solutions and at 4.35 in solutions containing 0.4 M KCl. In the presence of sodium molybdate, the sedimentation coefficients shifted both in the absence and presence of 0.4 M KCl to 8.9 and 5.7 S, respectively. The apparent equilibrium dissociation constants (Kd) of the glucocorticoid binding sites were similar in most tissues, ranging between 1 and 6 nM, with the exception of the placenta in which the binding sites showed a higher Kd (13-22 nM). In all tissues studied, the binding affinities were similar in nonpregnant and pregnant patients and in patients at different stages of pregnancy or in labor. The concentration of the binding sites in the different tissues ranged from 11 to 268 fmol/mg protein, higher concentrations being found in myometrium, placenta and amnion and lower concentrations found in endometrium, chorion and decidua. The number of binding sites was higher in the myometrium of nonpregnant than pregnant women, but was similar in the myometrium of women at term pregnancy before or during labor. In the placenta, the number of binding sites increased significantly from early pregnancy to midpregnancy, while in chorion, amnion and decidua the number of binding sites did not change during pregnancy. It is concluded that human uterine tissues, placenta and fetal membranes contain specific binding sites with properties characteristic of glucocorticoid receptors suggesting that these tissues may respond directly to glucocorticoids.

Amnion↗

PubMed1987

Modulation of phospholipase A2 activity in human endometrium and amniotic membrane by steroid hormones.

Phospholipase A2 (PLA2) activity was measured in endometrium and amnion by a double isotope ratio technique using 1-palmitoyl-2-oleoyl phosphatidylcholine as substrate in the presence and absence of a range of unconjugated steroids and steroid sulphates (0.2-6.4 X 10(-4) M). In the presence of 0.1% Triton, PLA2 activity was inhibited by the majority of steroids tested, pregnenolone sulphate being the most effective (12.9 +/- 3.0% control activity) while oestradiol sulphate, oestrone and testosterone had only a minimal or no effect (99.1 +/- 19.0, 85.4 +/- 4.4 and 104.2 +/- 16.3% control respectively). In the absence of Triton, the inhibitory effect of the free steroids was reduced or absent but oestradiol sulphate and testosterone sulphate stimulated activity by 2-13 and 1.5-3 times respectively. The effect was dose related, linear with time and independent of the stage of the menstrual cycle. Inhibition by pregnenolone sulphate, dehydroepiandrosterone (DHA sulphate and oestrone sulphate was maintained in the absence of Triton (24.9 +/- 3.8, 67.1 +/- 10.1 and 87.2 +/- 13.8% control respectively). In amnion all 5 steroid sulphates caused a marked stimulation of PLA2 activity in both the presence and absence of Triton. The effect was greatest without Triton and at 6.4 X 10(-4) M, testosterone, pregnenolone, oestrone, DHA and oestradiol sulphates increased PLA2 activity 20, 15, 12, 10 and 6-fold respectively. These findings indicate a direct action of steroid sulphates on PLA2 activity in endometrium and amnion.

Amnion↗

PubMed1993

Effects of interleukin-6 and tumor necrosis factor-alpha on prostaglandin production by cultured human fetal membranes.

In this study we investigated the effects of the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on prostaglandin production by cultured human fetal membranes. These cytokines stimulate prostaglandin synthesis by isolated components of human fetal membranes, but their effects on the intact tissue comprising amnion, chorion and decidua were not known. TNF-alpha added to the maternal side of the membrane activated decidual production of PGF2 alpha but had no effects on synthesis of PGE2 or PGE2 metabolites. Addition of TNF-alpha to the fetal side of the membrane increased production of PGE2 by amnion and PGE2 metabolites from chorion. The addition of IL-6 to the fetal or the maternal side of the membrane increased production of PGE2 from amnion and PGE2m from chorion, suggesting that IL-6 might pass through the fetal membrane. IL-6 had no effect on decidual PGF2 alpha production. These results suggest that TNF-alpha may be involved in labor by increasing decidual prostaglandin synthesis, whereas IL-6 is less likely to have a role.

Amnion↗

PubMed1996

5-Hydroxyeicosatetraenoic acid and human parturition.

5-Hydroxyeicosatetraenoic acid (5-HETE) is an arachidonic acid (AA) metabolite derived from the lipoxygenase pathway which is capable of inducing uterine contractions. The purpose of this study was to determine a). whether 5-HETE concentrations in amniotic fluid increase before or after the onset of labor and b). whether acetylsalicylic acid (ASA) could modulate the production of 5-HETE by human amnion cells. 5-HETE concentrations are increased in amniotic fluid before the onset of labor. Furthermore, ASA treatment as expected inhibited PGE2, but also significantly increased 5-HETE production by amnion cells. 5-HETE concentrations on average increased by greater than 2.5 fold (p < 0.001) in amniotic fluid prior to spontaneous labor when compared with samples obtained from the same patients earlier in gestation and therefore may be important in mechanisms regulating the onset of labor. ASA provokes an increase in 5-HETE biosynthesis by amnion cells: control media 2.60 +/- 1.5, ASA treatment alone 5.17 +/- 0.20, IL-1 beta alone 6.39 +/- 2.1, and ASA + IL-1 beta 8.95 +/- 1.2 (mean +/- SEM) picograms per microgram protein per 16 hours. These findings may explain in part why cyclooxygenase inhibitors are not always successful in treating women with preterm labor.

Amniocentesis↗

PubMed1979

The concentrations of the prostaglandins E and F, 13 14-dihydro-15-oxo-prostaglandin F and thromboxane B2. In tissues obtained from women with and without pre-eclampsia.

The concentrations of prostaglandins E (PGE) and F (PGF), 13, 14-dihydro-15-oxo-prostaglandin F (PGFM) and thromboxane B2 (TXB2) were measured by specific radioimmunoassays in tissues obtained from women with and without pre-eclampsia. The concentrations of PGE in the amnion, chorion, decidua and placenta obtained from subjects with pre-eclampsia were significantly lower than those from subjects without pre-eclampsia. The concentration of PGE in these tissues increased significantly with gestational age and correlated with urinary oestrogen excretion. PGF concentrations were lower in the amnion and placenta of the pre-eclamptics compared to those without pre-eclampsia. The concentrations of PGFM in the amnion, decidua, and myometrium were lower in the pre-eclamptics. No significant difference in the TXB2 concentrations between the two groups of subjects were found. It is suggested that the altered tissue concentrations of prostaglandins in pre-eclamptics are due to the effects of gestational age and oestrogens and may or may not be involved in the pathogenesis of pre-eclampsia.

Adolescent↗

PubMed1988

Topographical expression of class I major histocompatibility complex antigens on human amniotic epithelium.

The expression of class I major histocompatibility complex (MHC) antigens on different regions of human amnion was studied by the avidin-biotin-complex immunoperoxidase (ABC) technique using monoclonal antibodies. In contrast to previous reports, the use of higher affinity monoclonal antibodies and the sensitive immunoperoxidase method has allowed the identification of class I MHC antigens on the amniotic epithelium. The level of expression is different between cells from various parts of the amnion, with the amniotic epithelium from the edge of the placenta consistently showing the strongest reactivity. Some of the class I MHC antigens expressed by the amnion are similar to those expressed by extravillous trophoblast cells in that both show much weaker or no reactivity with the monoclonal antibody 61D2.

Amnion↗

PubMed2005

Pre-B-cell colony-enhancing factor is a secreted cytokine-like protein from the human amniotic epithelium.

OBJECTIVE: The purpose of this study was to determine whether pre-B-cell colony-enhancing factor is a secreted cytokine in the human amnion and to study its chemotaxic and antiapoptotic properties. STUDY DESIGN: Pre-B-cell colony-enhancing factor secretion was studied from amniotic epithelial-like WISH cells and primary amniotic epithelial cells that were seeded on squares of immobilon-P membrane and stimulated with lipopolysaccharide or tumor necrosis factor-alpha, respectively. The pre-B-cell colony-enhancing factor protein was detected both intracellularly and after secretion, as bound to the membrane, by immunostaining and densitometry. Medium and cell lysates that were obtained from WISH cells that were treated with lipopolysaccharide alone or together with a pre-B-cell colony-enhancing factor antisense oligonucleotide to block pre-B-cell colony-enhancing factor translation were also analyzed for secreted pre-B-cell colony-enhancing factor by Western blotting and densitometry. A chemotaxic effect of pre-B-cell colony-enhancing factor on human neutrophils was compared with the chemoattractants interleukin-8 and N-Formyl-Met-Leu-Phe methyl ester in a rapid fluorescence-based neutrophil migration assay. Apoptosis was induced in primary amniotic epithelial cells and fibroblasts by actinomycin D (1 microg/mL); the antiapoptotic effects of pre-B-cell colony-enhancing factor on early apoptosis were measured by the annexin V assay, and the late effects were determined by measurement of nuclear matrix protein in the media. RESULTS: Treatment of amnion cells that adhered to immobilon-P membrane to induce the secretion of pre-B-cell colony-enhancing factor showed significantly (P<.05) more pre-B-cell colony-enhancing factor protein surrounding the cells compared with the controls. Although the addition of lipopolysaccharide to cultured WISH cells caused the secretion of pre-B-cell colony-enhancing factor into the medium, co-treatment with an antisense oligonucleotide to pre-B-cell colony-enhancing factor obliterated it. Analysis of the cell lysates showed no significant change, which suggests that most of the pre-B-cell colony-enhancing factor protein had been secreted. No significant chemotaxic effects of pre-B-cell colony-enhancing factor were observed; however, pre-B-cell colony-enhancing factor treatment (100 ng/mL), together with actinomycin D, cancelled the early induction of apoptosis, although there was a dose-dependent and significant late antiapoptotic effect on primary amnion epithelial cells (P<.001) and fibroblasts (P<.01). CONCLUSION: Pre-B-cell colony-enhancing factor is a secreted protein from amniotic epithelial cells. Although it had no chemotaxic effects, it was antiapoptotic for both amniotic epithelial cells and fibroblasts and may protect these cells against apoptosis that is induced by chronic distension, labor, or infection.

Amnion↗

PubMed2005

A histological study of fetoscopic membrane defects to document membrane healing.

OBJECTIVE: To evaluate the rate of spontaneous healing in human fetal membranes after fetoscopy. STUDY DESIGN: Membranes from patients that had undergone fetoscopic interventions and delivered in one of the two treatment centers were included in the study. The membranes were examined macroscopically for any remaining defects and if present, the size of the defect in chorion and amnion was measured. Subsequently, the defect was excised and stained with HE for histological evaluation. Additional immunohistochemical staining was performed with Ki-67, cytokeratin and vimentin. The proliferation index (percentage of proliferating cells) was calculated in amnion and chorion. RESULTS: Nineteen membrane defects were included in the study. The median time interval between invasive procedures and delivery was 60 days (range 3-112). All fetoscopic defects (n=19) could be identified in the gestational sac and in none spontaneous closure had occurred. Proliferation indices as measured by inmunohistochemistry were very low (median 2.8%, range 0-7%) in the chorion and 0% in the amnion. CONCLUSION: No evidence of spontaneous membrane healing was found after fetoscopic procedures, suggesting that the membrane defect normally persists until delivery. Absence of amniotic fluid leakage after invasive procedures may be based on mechanisms other than histologic membrane repair.

Amnion↗

PubMed2000

Effective diminution of amniotic prostaglandin production by selective inhibitors of cyclooxygenase type 2.

OBJECTIVE: Cyclooxygenase inhibitors are effective tocolytic agents, but significant adverse effects limit their use. We hypothesized that selective inhibitors of the isozyme cyclooxygenase 2 would effectively diminish labor-associated prostaglandin production. STUDY DESIGN: We analyzed cyclooxygenase type 1 and 2 expression in amnion, chorion, decidua, and myometrium from laboring or nonlaboring women and tested the efficacy of selective cyclooxygenase 2 inhibition in diminishing prostaglandin production. RESULTS: The expression of cyclooxygenase 2 in amnion from women in labor, either preterm or at term, was significantly higher than in amnion before labor. In contrast, cyclooxygenase 1 expression was unchanged by labor. The enhanced expression of amniotic cyclooxygenase 2 was associated with increased prostaglandin E(2) levels in laboring women. Amniotic prostaglandin E(2) production was effectively diminished by the selective cyclooxygenase 2 inhibitors SC-236 and NS-398 but not by the cyclooxygenase 1 inhibitor SC-560. CONCLUSION: Selective inhibitors of cyclooxygenase 2 are effective in diminishing prostaglandin production in vitro and may be useful in prevention of preterm deliveries.

Amnion↗

PubMed1997

Collagenolytic enzymes (gelatinases) and their inhibitors in human amniochorionic membrane.

OBJECTIVE: This study was designed to investigate the presence of matrix metalloproteinase-2 (gelatinase A), matrix metalloproteinase-9 (gelatinase B), and their natural inhibitors in both cultured amniochorionic membrane and membrane obtained from women with infection-associated preterm labor. STUDY DESIGN: Amniochorionic membranes were collected from women with documented intraamniotic infection and from women not in labor undergoing elective repeat cesarean section with no signs of infection or other complications of pregnancy. Normal membranes were cultured and exposed to endotoxin and peptidoglycan polysaccharide. Messenger ribonucleic acid expression for gelatinase A, gelatinase B, and tissue inhibitors of matrix metalloproteinase types 1 and 2 was studied with use of reverse transcriptase-polymerase chain reaction and localization of messenger ribonucleic acid was accomplished with use of in situ hybridization. Release of gelatinases from the membranes was studied with gelatin zymography. Tissue inhibitors of matrix metalloproteinase peptides were localized with use of immunocytochemistry. RESULTS: The expression of matrix metalloproteinase types 2 and 9 was seen in amniochorionic membranes in culture. Matrix metalloproteinase-2 was seen in membranes from nonlaboring women and in women with intraamniotic infection, whereas matrix metalloproteinase-9 was seen only in membranes from women with intraamniotic infection. The matrix metalloproteinase-9 expression could also be induced by lipopolysaccharide or peptidoglycan polysaccharide stimulation in culture. In situ hybridization localized messenger ribonucleic acid for these matrix metalloproteinases to both amnion and chorion. Zymogram studies showed the activity of matrix metalloproteinase-2 in normal resting membrane and cultured membrane. Matrix metalloproteinase-9 was induced by culture conditions. Tissue inhibitor of matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-2 messenger ribonucleic acid was seen in normal, infected, and cultured membranes. In situ hybridization data indicated that these messages were mainly produced by chorion, but they were also seen in amnion. Immunohistochemistry demonstrated the presence of tissue inhibitor of matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-2 peptides in both amnion and chorion and in cells of the reticular layer of the matrix. CONCLUSION: Normal amniochorionic membrane is a source of matrix metalloproteinase-2 and tissue inhibitors of matrix metalloproteinases. Culture conditions and infection induce matrix metalloproteinase-9 expression and release from amniochorion. These findings suggest that these collagenolytic enzymes may play a role in premature rupture of the membranes in infection, which can lead to preterm labor.

Amnion↗

PubMed1998

In vitro studies of the interactions between platelets and amniotic membranes: a potential treatment for preterm premature rupture of the membranes.

OBJECTIVE: Thus far there is no satisfactory treatment for preterm premature rupture of the amniotic membranes. To evaluate the use of platelets to seal the membranes, we investigated in vitro interactions between platelets and the membranes. STUDY DESIGN: Platelet aggregation in the presence of amnion, chorion, and amniotic fluid was quantified. Platelet adhesion to the fetal membranes was investigated by electron microscopy. In addition, a model system was designed to evaluate the capacity of platelets to seal a standardized puncture in the membranes. RESULTS: Platelets aggregated in response to amnion but not to chorion or amniotic fluid. Adhesion and activation occurred on connective tissues underlying amnion and chorion but not on the amniotic epithelium. Platelets sealed a puncture in fetal membranes, and the platelet plug was visualized by electron microscopy. CONCLUSIONS: Exposed connective tissue of amniotic membranes was demonstrated to trigger platelet adhesion, aggregation, and activation, and platelets were shown to seal a standardized puncture in fetal membranes. Our results indicate that platelets might be useful for treatment of ruptured membranes after needle puncture.

Amnion↗

PubMed1996

Localization of type II phospholipase A2 messenger RNA and immunoactivity in human placenta and fetal membranes.

Although Type II phospholipase A2 (PLA2) immunoactivity has been identified in homogenates of human placenta and fetal membranes, there is a paucity of information concerning the sites of synthesis of this secreted PLA2 isozyme. The aim of this study, therefore, was to establish the cellular localization of Type II PLA2 messenger RNA (mRNA) in human term placental and fetal membranes by in situ hybridization. In addition, the co-localization of immunoreactive Type II PLA2 in gestational tissues was determined, and the effect of labour status and pre-eclampsia on immunolabelling intensity were established. Type II PLA2 mRNA was identified in all tissue sections examined and was localized principally in placental villous vasculature and mesenchymal elements of placenta, chorion and amnion. Within the vasculature, Type II PLA2 mRNA was associated with smooth muscle cells. Immunoreactive Type II PLA2 was identified in the fibroblast and spongy layers of the amnion, the fibroblast and reticular layer of the chorion, and in the mesenchymal core and trophoblasts of placental villi. Immunolabelling staining intensity was greater in placenta and chorion than that observed in amnion, however, staining intensity was unaffected by labour status. Pre-eclampsia was associated with increased immunolabelling for Type II PLA2 in placenta but not fetal membranes. The data obtained clearly established that Type II PLA2 is synthesized by multiple cell types within human gestational tissues and co-localization of Type II PLA2 mRNA and immunoreactive protein has been established. The role of Type II PLA2 in gestational tissue phospholipid metabolism and, in particular, in vascular and mesenchymal elements, has yet to be established. Possible roles for this isozyme may include, the provision of substrate for eicosanoid synthesis, maintaining cell membrane phospholipid asymmetry and prevention of clot formation within the placental vascular bed.

Amnion↗

PubMed1997

Lipoprotein lipase, LDL receptors and apo-lipoproteins in human fetal membranes at term.

Ultrastructurally, all cells of human fetal membranes strongly exhibit a large amount of lipid deposits throughout pregnancy. Their origin and function is still unknown. The aim of this study was to investigate the localization of key components of lipid metabolism in this tissue. Using immunohistochemical techniques, the distribution of lipoprotein lipase (LPL), low density lipoprotein receptors (LDL receptors), and apo-lipoprotein B and E was investigated in 20 human fetal membranes at term. In addition, electron microscopy was used to study the intracellular localization of lipoprotein-sized particles. Amnionic epithelium and trophoblast cells reacted strongly for LPL. LDL receptors and apo-lipoproteins were present in amnionic epithelium and fibroblasts of the amnion. In none of the investigated cells were lipoprotein-sized particles identified. Similar results were obtained in all 20 cases. The findings indicate that lipoprotein from the amniotic fluid or from the maternal circulation may serve as substrate for lipids in human fetal membranes.

Amnion↗

PubMed1989

Endothelial cell interactions with native surfaces.

Since native vessels are presumably the ideal surface for endothelial cells, we have examined endothelial cell interactions with natural surfaces as a standard to determine the possibilities obtainable on a surface. We have examined three separate types of natural surfaces including human amnion, superficially-injured human arteries, and tanned bovine carotid arteries. When basement membrane collagen is a principal component of a surface, such as with amnion or a superficially denuded large vessel, very rapid cell attachment and spreading occurs. Intact confluent monolayers covering 100% of the amnion surface are present as early as one hour. Human arteries superficially injured to denude their endothelium also exhibit excellent affinity for EC adherence and spreading. Endothelial monolayers cover 80.8% (+/- 5.3) of this surface after one hour, with 91.4% (+/- 1.2) coverage after two hours. For tanned bovine carotid arteries, one and two hour endothelial cell incubation results in coverage of 59.2% (+/- 1.3) and 75.9% (+/- 4.1), respectively. This surface is composed of interstitial collagen of the arterial wall in medial and adventitial layers. Electron microscopy reveals excellent endothelial cell spreading with little or no exposed underlying basement membrane. This suggests that polymeric surfaces designed to mimic injured native surface could allow an endothelialized surface to develop within minutes to hours.

Amnion↗

PubMed1996

Prostaglandins in selected reproductive tissues in preterm and full-term gestations.

We investigated differences in maternal plasma and trophoblast prostaglandin metabolism associated with preterm births. Tissue prostaglandins (PGs) E2 and F2 alpha and the stable plasma PGF2 alpha metabolite, 13,14-dihydro-15-keto-PGF2 alpha, were measured in preterm (< 37 weeks) and term (< or = 37 weeks) births. Amnion PGE2 in preterm (106.1 +/- 15.7 ng/g wet weight tissue; x +/- SEM; n = 37) was lower than in term (176.6 +/- 22.7 ng/g wet weight; x +/- SEM; n = 34, P < 0.02). Placenta PGE2 was lower in preterm (34.7 +/- 19.7 ng/g wet weight; x +/- SEM) than in term (103.3 +/- 28.0 ng/g wet weight; x +/- SEM, P < 0.04). Preterm PGF2 alpha was consistently lower in the amnion (106.8 +/- 17.5 ng/g wet weight) and placenta (102.5 +/- 8.7 ng/g wet weight) than in term amnion (188.2 +/- 24.8 ng/g wet weight; P < 0.01) and placenta (128.9 +/- 7.8 ng/g wet weight; P < 0.03). Chorionic PGE2 and plasma PGF2 alpha metabolite followed this trend but did not reach significance. These findings suggest qualitative and quantitative differences in maternal and trophoblast eicosanoid metabolism between term and preterm parturition.

Adult↗

PubMed2003

Effects of sex hormones, forskolin, and nicotine on choline acetyltransferase activity in human isolated placenta.

The activity of choline acetyltransferase (ChAT) was investigated in the human placenta before and after long-term incubation (24 h) to test the effects of sex hormones, nicotine and forskolin. ChAT activity differed considerably between the amnion (0.03 micromol/mg protein/h) and the villus (0.56). After long-term incubation, ChAT activity persisted in the latter but declined in the amnion. Neither sex hormones (beta-estradiol, testosterone, progesterone; 10 or 100 nM each) nor follicle stimulating hormone and luteinizing hormone (FSH/LH; 8.4 U/ml each) modified ChAT activity. Also nicotine (1 nM-100 microM) did not affect ChAT activity. Forskolin, an activitor of adenylyl cyclase, reduced ChAT activity in the villus but not in amnion. The present model offers the possibility to investigate ChAT regulation in intact tissue under long-term incubation. The risks of maternal smoking during pregnancy cannot be attributed to an effect of nicotine on placental ChAT activity. Differences in the regulation of ChAT appear to exist between neuronal and nonneuronal cells.

Amnion↗