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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have measured the levels of gonadotrophin-releasing hormone (GnRH) binding sites in human placental villous membrane fractions obtained at different stages of gestation. There was a marked decrease in the specific activity of 125I-labelled GnRH binding to membrane fractions obtained between 10-20 weeks gestation, but there was no change in either affinity or ligand specificity of these binding sites. The observed decrease in binding was not due to contamination of placental villous membranes by membranes from other tissues, since there was no gestation-dependent decrease in the specific activity of epidermal growth factor receptor or alkaline phosphatase activity in villous membrane fractions between 10-20 weeks of gestation. Furthermore, incubation of GnRH tracer with membranes from different stages of gestation, followed by re-incubation of the unbound tracer fraction with fresh membranes, demonstrated unequivocally that decreased GnRH binding to 10-20 week membranes was not due to increased degradation of GnRH tracer. We conclude that the observed changes in GnRH receptor levels between 10-20 weeks gestation must reflect either decreased expression/synthesis (or increased catabolism) of placental GnRH receptors, or increased occupancy (or down-regulation) of placental GnRH receptors by an endogenous GnRH-like ligand.
Placenta 1994 Oct
PMID:Human placental gonadotrophin-releasing hormone (GnRH) binding sites: III. Changes in GnRH binding levels with stage of gestation. 783 29

Human placental chorioepithelial brush border membrane, which is in direct contact with maternal blood flow, has platelet aggregation inhibiting activity. In the present study, the mechanism of this action has been examined in relation to ADP (adenosine diphosphate) degrading activity and alkaline phosphatase activity of brush border membrane vesicles (BBMV). BBMV prepared from human early and term placental villi, inhibited platelet aggregation induced by ADP. BBMV had potent ADP degrading (ADPase) activity. ADP was quickly degraded by BBMV. ADP degrading activity of BBMV was not so different between early and term placenta. Alkaline phosphatase activity of late placental BBMV was about three times greater than that of early placental BBMV. On the other hand, ADP degrading activity of late placental BBMV was almost the same as that of early placental BBMV. Inhibiting activity of platelet aggregation induced by ADP and ADP degrading activity of BBMV, were not inhibited by levamisole (alkaline phosphatase inhibitor).
Placenta 1994 Apr
PMID:Platelet aggregation inhibiting activity of human placental chorioepithelial brush border membrane vesicles--the role of alkaline phosphatase. 806 52

Human placental mitochondria prepared by a new isolation procedure exhibit low but well coupled rates of state 3 respiration with different substrates (succinate: 32.3 nmol O2/mg/min, RCI = 4.4; pyruvate: 12.6 nmol O2/mg/min, RCI R = 4.2; palmitoylcarnitine: 16.6 nmol O2/mg/min, RCI R = 4.9). The addition of the uncoupler FCCP increased the respiratory rates (succinate: 40.7 nmol O2/mg/min; pyruvate: 21.2 nmol O2/mg/min: palmitoylcarnitine: 25.4 nmol O2/mg/min). The low respiratory rates correlate well with a low capacity of the respiratory chain as shown by the specific contents of cytochrome c (0.15 nmol/mg), cytochrome b (0.19 nmol/mg) and cytochrome oxidase (0.14 nmol/mg) as well as with the low content of adenine nucleotides (2.71 nmol/mg). These data together with the finding of high activities of alkaline phosphatase (2.2 U/mg) support the view that human placental mitochondria are contaminated with nonmitochondrial membranes. Since it was not possible to obtain functionally intact mitochondria with negligible activities of alkaline phosphatase the influence of this enzyme on the extramitochondrial adenine nucleotide turnover was investigated. Alkaline phosphatase splits phosphate from ATP, ADP and AMP with different rates resulting in an intermediate accumulation of AMP. Mitochondrial adenylate kinase (0.16 U/mg) regenerated ADP from AMP and ATP resulting in drastically decreased ADP/O ratios and prolonged state 3 respirations. Inhibiting the adenylate kinase with diadenosine pentaphosphate the ADP regeneration from AMP and ATP was suppressed which, in turn, enhanced the ADP/O ratios. In the absence of magnesium ions, if both the alkaline phosphatase and the adenylate kinase are inhibited normal ADP/O ratios and state 3-state 4 transitions can be observed. Under these conditions, human placental mitochondria showed normal properties comparable to those of mitochondria from other tissues with the only exception of low specific activities.
Placenta 1994 Apr
PMID:Unusual properties of mitochondria from the human term placenta are caused by alkaline phosphatase. 806 53

Oxygen uptake in human placental mitochondria was stimulated by ATP addition. ATP-induced respiration was supported by malate, alpha-keto glutarate, and succinate, and inhibited by oligomycin and carboxytractyloside. This phenomenon was not caused by contamination with unspecific phosphatases or alkaline phosphatase, since NaF, L-phenyl alanine, or P1, P5-di-(adenosine-5') pentaphosphate failed to inhibit oxygen uptake induced by ATP. The stimulation of respiration was caused by an ATPase activity tightly bound to mitochondria, which yields ADP that is responsible for the oxygen uptake. The stimulation was not an uncoupling effect because ATP addition produced a transition between state 3 and 4 of respiration, indicating that ATP was not released from mitochondria.
Placenta
PMID:Respiratory control induced by ATP in human term placental mitochondria. 836 13

The expression of insulin-like growth factor-II (IGF-II) in normal human first and third trimester placental tissue was investigated by non-isotopic in situ hybridization (ISH). This is the first ISH study on IGF-II expression in placenta using an alkaline phosphatase-labelled probe. The expression was correlated with the proliferative activity of the cells using the proliferative marker MIB-1. In first trimester tissue, IGF-II was expressed in the cytotrophoblast, the extravillous trophoblast, the fetal endothelial cells and the mesenchymal fetal cells in the villi. In third trimester tissue, IGF-II expression was found in the amnion, the extravillous trophoblast and the mesenchymal fetal cells especially in the endothelial cells and the outer contractile sheet in the stem villi. In areas with perivillous fibrin deposits, strong expression of IGF-II was found in the cytotrophoblasts invading the fibrin. In first trimester tissue, the proliferative activity of the villous cytotrophoblast correlated well with the degree of IGF-II expression whereas in third trimester tissue, there was a discrepancy between MIB-1 positivity and the IGF-II expression. Expression of IGF-II does not seem to be correlated exclusively to the mitogenic activity of cells.
Placenta
PMID:Patterns in expression of insulin-like growth factor-II and of proliferative activity in the normal human first and third trimester placenta demonstrated by non-isotopic in situ hybridization and immunohistochemical staining for MIB-1. 908 75

The purpose of this study was to examine evidence for the presence of activated leukocytes in the fetal membranes from patients with preterm delivery. Polymorphonuclear leukocytes in fetal membranes from seven patients with preterm delivery (26-32 weeks of gestation) were analysed using transmission electron microscopy and ultrastructural enzyme-histochemistry for peroxidase and alkaline phosphatase. A large number of leukocytes accumulated in the fetal membranes from preterm deliveries. Phagosome, phagocytosis of cell debris, attachment of primary granules to the phagosomal membrane and cell surface projections were observed in fetal membrane leukocytes from preterm delivery but not in peripheral blood leukocytes. Peroxidase and alkaline phosphatase activity was demonstrated on the plasma membrane of the phagosomes. Morphological and enzyme-histochemical observation indicated that polymorphonuclear leukocytes in the fetal membrane in patients with preterm delivery were stimulated or activated. Such activated leukocytes may play a role in the pathophysiology or pathogenesis of preterm delivery.
Placenta
PMID:Polymorphonuclear leukocytes in the fetal membranes are activated in patients with preterm delivery: ultrastructural and enzyme-histochemical evidence. 1019 40

In mice and humans, expression of the tumour necrosis factor receptor-1 (TNF-R1) gene in placental trophoblast cells is constitutive whereas expression of the TNF-R2 gene is developmentally programmed. In order to study the individual functions of TNF-R1 and -R2 in this lineage, cell lines were generated from placental explants of homozygous matings of gestation day 10 outbred mice (Swiss-Webster), TNF-R1-deficient (TNF-R1-/-) and TNF-R2-/- transgenic mice as well as the background strain for the TNF-R2-/- mice (WT, C57BL/6x129). All of the cells exhibited trophoblast markers; they contained cytokeratin intermediate filaments, expressed alkaline phosphatase activity and displayed transferrin receptors, but were negative for vimentin filaments and the macrophage marker, F4/80. Analysis of DNA by polymerase chain reaction demonstrated the expected TNF-R genotype in each line. In experiments testing the effects of recombinant mouse TNF-alpha (rmTNF-alpha) on viability and proliferation of the cell lines, rmTNF-alpha modestly but dose-dependently inhibited the growth of WT and TNF-R2-/- cells while having no effect on TNF-R1-/- cells. Actinomycin D-treated WT and, to a lesser extent, TNF-R2-/- cells, were more sensitive to growth inhibition than untreated cells whereas TNF-R1-/- cell responses remained unchanged. These data indicated that rmTNF-alpha inhibits growth of trophoblastic cells through TNF-R1 and that newly synthesized protein(s) provide partial protection against toxicity. In contrast to the receptor species-specific effects on cell growth exerted by rmTNF-alpha, both TNF-R mediated inhibition of alkaline phosphatase activity. Collectively, the observations support the postulate that receptor expression is the key factor which determines the nature and extent of TNF-alpha effects on trophoblast cell growth and function.
Placenta
PMID:Trophoblastic cell lines generated from tumour necrosis factor receptor-deficient mice reveal specific functions for the two tumour necrosis factor receptors. 1019 44

Vitamin A and retinoids play an important role during development. They affect morphogenesis, cell growth and differentiation by interacting with two types of receptor, the RARs and the RXRs. Despite the well known established teratogenic effects of retinoids during human pregnancy, little is known about the effect of retinoids on human placental development. We studied the possible involvement of retinoids during the implantation process by investigating the spatial distribution of retinoid receptors in the human implantation site by in situ hybridization and immunohistochemistry. For in situ hybridization, we used digoxigenin-labelled antisense riboprobes. Immunochemical staining was performed with specific antibodies against the various retinoid receptors and a streptavidin-alkaline phosphatase immunostaining kit. We found that only two types of receptors were expressed at the implantation site: RARalpha and RXRalpha. Both types of receptors were present in the proliferative intermediate trophoblast, the invasive extravillous trophoblast and decidual cells. Both receptors were also present in the villous cytotrophoblasts. The presence of this retinoid receptor in the cytotrophoblasts suggests a key role for all-trans retinoic acid and/or 9-cis retinoic acid in the development of human placenta.
Placenta 2000 Sep
PMID:The expression of nuclear retinoid receptors in human implantation. 1098 74

We localized alkaline phosphatase and plasma membrane calcium-ATPase (PMCA) in the cat placental syncytiotrophoblast to address their polarized distribution and their potential as markers for specific plasma membrane purification. We used enzyme- (alkaline phosphatase) and immuno- (PMCA) histochemistry and, for alkaline phosphatase, compared data to observations on the human placenta. Alkaline phosphatase activity in the cat was localized to the decidual cell membranes, to within the associated interstitial space and on the subjacent apical (maternal facing) plasma membrane of the syncytiotrophoblast. Occasional maternal capillaries were positive on their basal surface and there was focal staining within the syncytiotrophoblast. This widespread distribution is less specific than in the human placenta where alkaline phosphatase was restricted to the apical and basal plasma syncytiotrophoblast membranes, with much greater density on the apical membrane. Expression of PMCA in the cat was restricted to the basal membrane of the syncytiotrophoblast only. This specific localization of PMCA is identical to the human placenta and all other species in which its placental localization has been studied. We conclude that the plasma membranes of the cat syncytiotrophoblast show a broadly similar functional polarization to the human and that PMCA would prove a useful marker in isolation of the cat syncytiotrophoblast basal plasma membrane.
Placenta 2003 May
PMID:Localization of alkaline phosphatase and Ca2+-ATPase in the cat placenta. 1274 21

Human placental syncytiotrophoblast is the main barrier for materno-fetal exchange. Analysis of transplacental transport involves the study of ion channels in both the maternal-facing microvillous membrane (MVM) and the fetal-facing basal membrane (BM). Difficulties in having access to intact placenta with conventional electrophysiological methods favour alternative methodologies, such as isolation and reconstitution of membranes in artificial lipid systems. Pre-eclampsia is a major health problem of human pregnancy. The search for altered physiological processes in pre-eclamptic placentae requires the investigation of events at both the microvillous and basal surfaces. The aim of this study was to obtain reliable syncytiotrophoblast plasma membranes from human normal (N) and pre-eclamptic (PE) pregnancies. We describe a protocol which allows for the simultaneous isolation of MVM and BM. The purity of the membranes isolated was evaluated using enzymatic assays, binding studies, Western blotting and immunohistochemistry. Enrichment of alkaline phosphatase activity for MVM was 17 to 21-fold, with 13-16 per cent protein recovery, for both N and PE. Enrichment of adenylate cyclase activity for BM was 9-fold for N, and enrichment of dihydroalprenolol binding to beta-adrenergic receptors was 12-fold for N and 6-fold for PE, with 14 per cent protein recovery for both N and PE. Cross contamination was low and mitochondrial membrane contamination was negligible. We conclude that MVM and BM isolated from placentae of pre-eclamptic women are similar in enrichment and purity to those of healthy women, thus allowing their use in comparative electrophysiological studies.
Placenta 2004 May
PMID:Isolation and purification of human placental plasma membranes from normal and pre-eclamptic pregnancies. a comparative study. 1508 37


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