Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed2003

"Amnion Bank"--the use of long term glycerol preserved amniotic membranes in the management of superficial and superficial partial thickness burns.

With about 2 million cases of burns in India of which about 90% are superficial and superficial partial thickness burns, burn injuries present a major challenge to the scarce medical resources available. The main requirement in treating these burns is an economical, easy to apply, readily available dressing that will provide good pain relief, protect the wound from infection, promote healing, prevent heat and fluid loss, be elastic and non-antigenic and adhere well to the wound. It was in the quest of such an ideal dressing that the Burn Centre of the Army Hospital (Research and Referral) New Delhi, India has been using human amniotic membranes preserved long term in 85% glycerol for treating these wounds. The results of this quest have resulted in a protocol where these long term glycerol preserved membranes (some of which have now been preserved for about 2.5 years) are used for treating superficial and superficial thickness burns presenting at our center. This paper shows the excellent results obtained with the use of this extremely economical dressing and emphasizes the importance of establishing such "Amnion Banks" in all hospitals especially in developing countries.

Amnion↗
PubMed1998

Interleukin-1 beta and dexamethasone regulate gene expression of prostaglandin H synthase-2 via the NF-kB pathway in human amnion derived WISH cells.

Interleukin-1beta (IL-1beta) stimulated PGE2 synthesis in human amnion derived WISH cells, whereas dexamethasone blocked IL-1beta-mediated stimulation of PGE2 production. Sequence analysis of the 5'-flanking region of the human prostaglandin H synthase-2 (PGHS-2) gene indicates two putative NF-kB binding sites. Mutation of a single site or both sites resulted in significantly decreased activity of the PGHS-2 promoter. IL-1beta treatment increased significantly the native promoter activity and this increase was attenuated by using the NF-kB-mutant promoter. Dexamethasone treatment also decreased the IL-1beta mediated stimulation of the PGHS-2 native promoter but not the NF-kB mutant promoter. Furthermore, the involvement of the NF-kB was supported by electrophoretic mobility shift assay which revealed an increased nuclear binding of the NF-kB probe upon IL-1beta induction and a decreased nuclear binding of the NF-kB probe upon dexamethasone pre-treatment. These results provide convincing evidence that NF-kB may mediate the IL-1beta stimulation of PGHS-2 gene expression as well as the dexamethasone inhibition of the IL-1beta induction process in WISH cells.

5' Untranslated Regions↗
PubMed2003

Effects of conjugated linoleic acid on prostaglandins produced by cells isolated from maternal intercotyledonary endometrium, fetal allantochorion and amnion in late pregnant ewes.

The anticarcinogenic properties of conjugated linoleic acid (CLA) are, at least partially, attributed to its ability to interrupt the n-6 polyunsaturated fatty acid (PUFA) metabolic pathway for the biosynthesis of eicosanoids, including prostaglandins (PG). Both PGE(2) and PGF(2alpha) play key roles in parturition. In the present study, we compared the effects of CLA (a mixture of cis- and trans-9, 11- and -10, 12-octadecadienoic acid) and linoleic acid (LA) on PG production by cells isolated from maternal intercotyledonary endometrium, fetal allantochorion and amnion from late pregnant ewes. The results demonstrated that supplementation of LA and CLA significantly affected both the proportions and the amounts of PGs produced by all three tissue types. The ability of the uterus and placenta to respond to oxytocin (OT, endometrium only) and lipopolysaccharide (LPS) was also affected. LA inhibited PGE(2) and PGF(2alpha) production in the absence or presence of either oxytocin or LPS. In endometrial cells with or without oxytocin or LPS, CLA dose-dependently suppressed PGF(2alpha) generation, whereas low doses of CLA (20 microM) increased PGE(2) generation. Supplementation with CLA therefore increased the PGE(2)/PGF(2alpha) ratio in the endometrial cells. These results suggest that dietary supplementation of LA or CLA may affect both the initiation and progression of parturition.

Allantois↗
PubMed2004

The influence of different preservation and sterilisation steps on the histological properties of amnion allografts--light and scanning electron microscopic studies.

Despite thorough donor screening and preparation under aseptic conditions, conventional methods of preservation do not exclude the probability of a contamination with pathogenic germs. The purpose of this study was to investigate the changes of histological parameters of amnion transplants (ATs) through different methods of sterilisation and preservation. Therefore 10 different procedures for sterilisation and preservation of ATs were described. Specimens of each group were studied using different histological procedures such as light microscopy and scanning electron microscopy. General staining (Haematoxylin-eosin stain, periodic-acid-Schiff, Domack) and immunohistochemical methods have been applied in order to gain additional information concerning the structure of the amniotic epithelium and the basement membrane but also the distribution of collagens and intermediate filaments. Furthermore, the measurement of the ATs thickness was included in order to study the influence of the manufacturing procedures to this property. As a result we found that the histological appearance of the ATs is closely related to the applied sterilisation and preservation procedures. Although the basement membrane remained intact, especially the amniotic epithelium was partially destroyed by irradiation sterilisation. Further, the dissolution of the connective tissue layers into single fibre bundles was clearly visible. Procedures with and without peracetic acid sterilisation (PAA) preserved the tissue structure. Our results showed a significant variation in the tissue's thickness after different preservation procedures. Air- and freeze-dried ATs were found to be the thinnest tissues varying from 20 to 30 microm, the thickest ATs preserved in glycerol varied from 45 to 50 microm. Because ATs showed a preserved tissue structure after PAA sterilisation it can be recommended as an alternative for methods previously described in literature. Depending on the specific use of the AT one may choose from thinner or thicker allografts.

Amnion↗
PubMed1997

Rapid and transient induction of cyclo-oxygenase 2 by epidermal growth factor in human amnion-derived WISH cells.

The central enzyme in the prostaglandin (PG) biosynthetic cascade is PGH2 synthase or cyclo-oxygenase (COX). At present, two distinct isoforms of PGH2 synthase/COX have been identified: COX-1 and COX-2. In many systems, COX-1 is a constitutively expressed isoform that is responsible for normal physiological production of PGs, whereas COX-2 is an inducible isoform that responds to cytokines, endotoxin and growth factors by producing high levels of PGs. The regulation of COX-2 mRNA and protein, and the subsequent production of PGE2, were therefore examined in amnion-derived WISH cells stimulated with epidermal growth factor (EGF). Treatment of WISH cells with EGF (0.01-100 ng/ml) elicited dose-dependent synthesis of COX-2 mRNA and protein de novo. In addition, stimulation of WISH cells with EGF (10 ng/ml) induced steady-state levels of COX-2 mRNA and protein that appeared within 30 min and then declined rapidly to near baseline levels within 2-4 h. In contrast, COX-1 protein was unchanged in response to treatment with EGF. PGE2 production was also rapid and transient. Preincubation of cells with the novel COX-2 enzymic inhibitor NS-398 (10(-5)-10(-10) M) completely prevented PGE2 formation in a dose-dependent manner. Preincubation of cells in dexamethasone (Dex; 0.1 microM), however, resulted in only a 31% decrease in PGE2 formation in response to EGF (10 ng/ml) while completely attenuating PGE2 biosynthesis in tumour necrosis factor alpha (TNF-alpha)-stimulated cells. In addition, Dex (0.1 microM) was only partly effective at preventing EGF-induced COX-2 mRNA and protein expression de novo, whereas Dex completely inhibited TNF-alpha-promoted COX-2 mRNA and protein expression. Thus the results presented here demonstrate that EGF induces the rapid but transient expression of COX-2 mRNA and protein and the subsequent production of PGE2 in WISH cells.

Amnion↗
PubMed1996

Determination of renin, angiotensin converting enzyme and angiotensin II levels in human placenta, chorion and amnion from women with pregnancy induced hypertension.

OBJECTIVE: Pregnancy induced hypertension has been shown to be associated with a normal or low activity of the maternal circulating renin-angiotensin system (RAS) but little is known of the local RAS in placenta and fetal membranes. The present study attempts to determine, at full term of human preeclamptic pregnancies, the activity of the chorioplacental renin-angiotensin system. PATIENTS AND MEASUREMENTS: We analysed the concentrations of active renin, prorenin, angiotensin converting enzyme (ACE) and angiotensin II in homogenates of human placenta and fetal membranes from preeclamptic patients at full term pregnancy. The values of renin, ACE and angiotensin II found in the patients with moderate preeclampsia (gestosis index 0-1) (n = 10) were compared with those of normal pregnant women (n = 8). RESULTS: Our experiments showed that in preeclamptic pregnancies, the chorion membrane contained the highest concentrations of active renin (2905 +/- 152 pg/g, mean +/- SD), prorenin (21,315 +/- 2849 pg/g) and ACE (1258 +/- 302 U/g) whereas the placenta had more angiotensin II than the chorion and amnion (741 +/- 45 vs 456 +/- 40 and 428 +/- 64 pg/g, respectively). In the placenta, as in the fetal membranes, no significant difference was found in the levels of active renin, ACE or angiotensin II between hypertensive patients and normal subjects but a slightly lower level of chorionic prorenin (P < 0.05) was observed in pregnancy induced hypertension. CONCLUSION: These findings indicate that in moderate preeclampsia (gestosis index 0-1), the activity of the renin-angiotensin system in term human placenta and fetal membranes remains essentially normal.

Amnion↗
PubMedDate not supplied

Effect of nitric oxide on arachidonic acid release from human amnion-like WISH cells.

In order to clarify the possible interactions between nitric oxide (NO) and arachidonic acid (AA) pathways, human amnion-like WISH cells were perifused to measure the effects of the following substances on [(3)H]arachidonic acid release: (1) sodium nitroprusside (SNP), a nitric oxide donor; (2) 1,1,1-trifluoromethyl-6,9,12,15-heicosatetraen-2-one, a cytosolic phospholipase A(2) (cPLA(2)) inhibitor; (3)L -arginine, the substrate of nitric oxide synthase (NOS); (4) 3-(5'-Hydroxymethyl-2'-furyl)-1-benzylindazole and 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one, activator and inhibitor of soluble guanylyl cyclase, respectively; (5) a membrane-permeable non-hydrolyzable analogue of guanosine-3',5'-cyclic monophosphate (cGMP). Furthermore, the effect of SNP on prostaglandin E(2) (PGE(2)) release was tested. Exogenous and endogenous NO, as well as the guanylyl cyclase activator and cGMP analogue, significantly increased [(3)H]arachidonic acid release. Both soluble guanylyl cyclase and PLA(2) inhibitors counteracted SNP response. Exogenous NO increased PGE(2) release, although to a much lesser degree compared with arachidonic acid release. Our results indicate that NO stimulates AA release in WISH cells by activating PLA(2) through a cyclic GMP-dependent mechanism.

Amnion↗
PubMed2000

Subcellular localization of prostaglandin H synthase-2 in a human amnion cell line: implications for nuclear localized prostaglandin signaling pathways.

We have determined that prostaglandin H synthase-2 localises strongly to the nuclear membrane as well as being found in the endoplasmic reticulum in human amnion-derived WISH cells which have been stimulated with interleukin 1beta and phorbol ester. This is consistent with findings in cells of non-reproductive origin. There is strong evidence that prostaglandin J2 derivatives, which in other tissues exhibit tumour suppressing, antiproliferative and/or differentiation promoting activities, act through binding of intracellular receptors which then enter the nucleus. In addition, some arachidonic acid derivatives are clearly generated by enzymes at the nuclear envelope and localise to sites in nuclei or bind sites in nuclei. The WISH cell line will make an excellent system for studying these perinuclear intracellular prostanoid signaling mechanisms.

Amnion↗
PubMed1991

Regulation of prostaglandin synthesis in the human amnion.

An increase in prostaglandin synthesis by intrauterine tissues may be responsible for labour initiation and/or maintenance in humans. In all studies to date, the amnion is the intrauterine tissue whose prostaglandin output consistently increases with the onset of labour. This may be due, in part, to acute activation of the phospholipases A2 and C and to an increase in the specific activity of prostaglandin H synthase (PGHS). A number of factors exist in amniotic fluid, the fetal membranes, the decidua and the placenta that can increase PGHS specific activity. Some of these factors may increase PGHS enzyme activity by gene expression and protein synthesis. Preliminary evidence is presented that suggests the hypothesis that PGHS specific activity increases before the onset of labour rather than as a consequence of labour initiation, and that idiopathic preterm labour may frequently be associated with increased PGHS activity. Hence, activation of PGHS gene expression and/or protein synthesis may be causal for term and preterm labour.

Amnion↗
PubMed1995

Studies on glucocorticoid hormone actions in the regulation of human amnion PGHS.

The human amnion is an excellent model in which to study the regulation of the expression of prostaglandin endoperoxide H synthase-2 (PGHS-2) mRNA by glucocorticoids, as glucocorticoids can both stimulate and inhibit PGHS activity and can have their stimulatory effect reversed to an inhibitory one. Our studies suggest the presence of a glucocorticoid-induced inhibitory protein which affects the post-transcriptional activity of PGHS-2 mRNA. Glucocorticoid-induced expression of PGHS-2 mRNA may be dependent on protein phosphorylation.

Amnion↗
PubMed1990

Increased phosphorylation of elongation factor 2 during mitosis in transformed human amnion cells correlates with a decreased rate of protein synthesis.

Elongation factor 2 was identified in the two-dimensional gel patterns of asynchronous human amnion cells (AMA) by comigration with purified rabbit reticulocyte elongation factor 2 and by two-dimensional gel immunoblot analysis using a specific rabbit polyclonal antibody. In all, four polypeptides were identified corresponding to isoelectric focusing polypeptides 2713 (95.0 kDa), 2714 (94.8 kDa), 3727 (94.8 kDa), and 3702 (93.6 kDa) (listed in order of decreasing pI values) in the computerized comprehensive two-dimensional gel data base of human AMA proteins. The relative proportion of two of these variants (isoelectric focusing polypeptides 3727 and 3702), which are phosphorylated, increased dramatically during mitosis. Since phosphorylation is known to render elongation factor 2 inactive in translation, this observation may partly explain the decline in the rate of protein synthesis observed during cell division.

Amnion↗
PubMed2005

The effect of epidermal growth factor on production of vascular endothelial growth factor by amnion-derived (WISH) cells.

Our objective was to clarify the physiological role of vascular endothelial growth factor (VEGF) by amnion-derived (WISH) cells. WISH cells were cultured, and the effect of epidermal growth factor (EGF), mitogen-activated protein (MAP) kinase kinase or extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitors (U0126) or phosphatidylinositol (PI) 3-kinase on the production of VEGF was examined. VEGF was assayed by ELISA. The activation of MAP kinase and akt, which is phosphorylated by PI 3-kinase, were detected by Western blot analysis using anti-phosphorylated MAP kinase antibody and anti-phosphorylated akt antibody. In the time course of VEGF production following EGF treatment, VEGF production showed a significant increase only after 16 (p < 0.01)-32h (p < 0.01). EGF increased the production of VEGF by WISH cells in a dose-dependent manner. The MAP kinase and akt activity were determined by treatment with EGF. VEGF production was significantly decreased following pretreatment with U0126 or wortmannin for two hours before treatment with EGF (p < 0.01, p < 0.01). WISH cells appeared to produce VEGF via a mechanism involving tyrosine kinase activation of EGF receptor and MAP kinase or PI 3-kinase. It is suggested that VEGF may contribute to the neovascularization and proliferation of the placenta and gestational tissue, and EGF may play an important role in regulation of VEGF production in the placenta.

Amnion↗
PubMed2004

Localization of alpha-tocopherol transfer protein in trophoblast, fetal capillaries' endothelium and amnion epithelium of human term placenta.

Vitamin E has been linked to fertility since its discovery in 1922. However, the exact mechanism by which alpha-tocopherol allows pregnancy to continue until term has remained puzzling over the last 80 years. Alpha-tocopherol transfer protein (TTPA) is expressed in liver and in Purkinje cells of the cerebellum. TTPA is suggested to be responsible for the transfer of alpha-tocopherol across barrier membranes. Ttpa-knockout mice are infertile and show symptoms similar to those observed in severe vitamin E deficiency. We thus investigated TTPA expression in human placenta and whether clues from its localization in different parts of the placenta might be of functional significance. TTPA-mRNA transcripts were quantified with a fluorescent 5'-nuclease assay (TaqMan) in five different tissues. Placental expression ranged second behind that of liver. Immunohistochemistry identified TTPA in the cytosol but also in nuclei of the trophoblast and in the endothelium of the fetal capillaries. Expression in trophoblast and fetal capillaries' endothelium indicates a role of TTPA in the stereoselective transport of RRR-alpha-tocopherol from the maternal to the fetal plasma. In amnion epithelial cells, however, TTPA was predominantly located in the nuclei. Nuclear localization of the protein may represent a novel function of TTPA.

Amnion↗
PubMed2005

Unique suppression of prostaglandin H synthase-2 expression by inhibition of histone deacetylation, specifically in human amnion but not adjacent choriodecidua.

The key molecular regulatory mechanisms that govern and coordinate the molecular alterations that underpin the process of human labor remain incompletely understood although enhanced intrauterine prostaglandin production is known to be requisite. Studies from cancer tissues have indicated that at least one key enzyme of prostaglandin biosynthesis can have its activity severely reduced by increased histone deacetylation and enhanced DNA methylation status. We have advanced the hypothesis that similar regulation may occur in intrauterine tissues during pregnancy to prevent inadvertent activation of this powerful initiating signal by dampening responses to premature activation by agents such as cytokines. Our studies have shown that responsiveness of amnion, a key intrauterine tissue, to interleukin-1beta is abrogated by inhibition of histone deacetylation, whereas PGDH amounts were increased basally. The findings do integrate well with others concerning progesterone (inhibitory) actions such that a decrease in the level of histone acetylation in human gestational tissues near term might herald a coordinated series of events that all result in a positive drive for parturition. Hence, a new level of regulatory action and potential therapeutic targets for pathologies such as preterm labor can flow from these findings.

Acetylation↗
PubMed2000

NF-kappaB and AP-1 are required for cyclo-oxygenase 2 gene expression in amnion epithelial cell line (WISH).

Prostaglandins are known to play an important role in human labour and are used clinically to induce labour onset. Cytokines, e.g. interleukin 1 beta (IL-1beta), are up-regulated in the amniotic fluid late in gestation and can increase prostaglandin production through the expression of cyclo-oxygenase 2 (COX-2), the prostaglandin synthetic isoform involved in human labour. We demonstrate in immortalized amnion epithelial (WISH) cells, that IL-1beta causes increased transcription of the COX-2 gene. Luciferase reporter constructs with site-directed mutagenesis of the two NF-kappaB sites and an AP-1 site in the COX-2 promoter showed reduced expression of luciferase in transient transfection studies. This suggests that the binding of transcription factors to these sites is essential for the regulation of COX-2 transcription in IL-1beta-treated WISH cells.

Amnion↗
PubMed2001

Nuclear factor-kappa B is essential for up-regulation of interleukin-8 expression in human amnion and cervical epithelial cells.

Interleukin-8 (IL-8) is a cytokine which recruits and activates neutrophils into tissue stroma. It is present in uterine tissues and its concentration increases in the third trimester and with labour. The promoter region of the IL-8 gene contains binding sites for the transcription factors, nuclear factor-kappa B (NF-kappaB), activator protein-1 (AP-1) and CCAAT/enhancer-binding protein (C/EBP). These are in close proximity to each other and to the coding region of the gene. This study used site-directed mutagenesis of each of these sites to examine the relative importance of each site in IL-8 gene expression in a cervical cell line and in amnion cells obtained before and after labour. We found that the NF-kappaB site was essential for basal and IL-1beta-stimulated gene expression in all cell types. Neither of the other binding sites was consistently essential for gene expression but may have an additive role in promoter activity. We conclude that the NF-kappaB binding site is essential for up-regulation of IL-8 gene expression in these uterine cell types. An increase in IL-8 expression has been shown to occur in the uterus in association with parturition and NF-kappaB binding to the promoter may be of importance at this time.

Amnion↗
PubMed2003

Endothelin-1 and macrophage colony-stimulating factor are co-localized in human amnion membrane cells and secreted into amniotic fluid.

We have examined the cellular localization and human amniotic fluid content of endothelin-1 (ET-1) and macrophage colony-stimulating factor (M-CSF). The study material consisted of amniotic fluid from 20 patients referred for amniocentesis, and placental samples from normal deliveries. ET-1 and M-CSF were analysed by radioimmunoassay and enzyme-linked immunosorbent assay respectively. The cellular localization of ET-1 and M-CSF in the amnion membranes was analysed by double-labelling immunocytochemistry using fluorescein isothiocyanate- and Cy3-labelled secondary antibodies. Release of ET-1 and M-CSF was studied in cultured amniocytes. We found that the mean +/- SD concentrations of ET-1 and M-CSF in fetal amniotic fluid were 45.6 +/- 17.3 pmol/l (range 16.8-85.5) and 7323 +/- 3415 ng/l (range 2640-12 110) respectively. Double-labelling immunocytochemistry showed that both M-CSF and ET-1 were co-localized in the same cells to a high extent. Further analysis revealed that levels of M-CSF, but not ET-1, were significantly correlated with pregnancy length. Both M-CSF and ET-1 were released from cultured amniocytes in response to interleukin-1. These findings show that ET-1 and M-CSF are partly co-localized to specific cells in the human amniotic membrane. As both M-CSF and ET-1 were released from cultured amniocytes in vitro, this suggests that they both may be secreted into fetal amniotic fluid in vivo as well.

Adolescent↗
PubMed2001

17beta-estradiol modulates prostaglandin E2 release from human amnion-derived wish cells.

In human amnion-derived WISH cells [(3)H]estradiol-17beta binding sites are not detectable, but they become measurable in cells exposed to cAMP elevating agents such as forskolin or Ro 20-1724. In cells unexposed to these drugs, 17beta-estradiol stimulates prostaglandin (PG)E(2) release but exerts an evident inhibitory effect in cells exposed to Ro 20-1724. Both stimulatory and inhibitory actions are inhibited by the estrogen receptor antagonist, tamoxifen, by cell pretreatment with cycloheximide, or when the hormone is bound to BSA. Our data demonstrate for the first time that 1) 17beta-estradiol modulates PGE(2) release from WISH cells, interacting with specific intracellular receptors and probably evoking new protein synthesis, and 2) WISH cell responsiveness to 17beta-estradiol seems to be modulated by cAMP, whose levels are significantly increased by the steroid hormone in the presence of Ro 20-1724. The nucleotide is presumably responsible for the enhacement of hormone receptor availability and for the inhibition of PGE(2) release observed in the presence of Ro 20-1724.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗