Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Placentation”

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 127 records · Page 7Linked to original sources
PubMedDate not supplied

Fetal-placental and decidual-placental units: role of endocrine and paracrine regulations in parturition.

In primates, fetal adrenal and placental steroidogenic enzymatic systems are complementary in a fetal-placental unit, synchronizing fetal maturation and myometrial activation in late gestation. Moreover, as hemochorial placentation characterizes rodents and primates, paracrine regulations between decidua and placenta are essential to the immunotolerance of the conceptus and its development. Thus, the decidual-placental unit remains in a striking state of decidual quiescence throughout gestation, and the reversal of this quiescence is thought to play a key role in myometrial stimulation and the onset of parturition. A comprehensive view of the control of myometrial contractility, through the interaction of paracrine and endocrine modifications in late gestation, is proposed. The failure of these mechanisms underlie prematurity and the use of fetal therapy in threatened preterm labor.

Animals↗
PubMed1997

Maternal growth hormone treatment increases placental diffusion capacity but not fetal or placental growth in sheep.

We tested the hypothesis that chronic maternal GH administration would increase fetal substrate supply, increase maternal and fetal insulin-like growth factor I (IGF-I) concentrations, and therefore enhance growth in the late gestation fetal sheep. Eleven ewes received bovine GH 0.1 mg/kg twice daily for 10 days, whereas 10 control ewes received saline. GH treatment increased placental capacity for simple diffusion (P < 0.01), with a trend toward an increase in placental capacity for facilitated diffusion (P = 0.07). GH treatment also lowered maternal and fetal blood urea concentrations, and there was a trend toward increased fetal protein oxidation (P = 0.07). Maternal but not fetal IGF-I and insulin concentrations increased. Fetal and placental growth were not altered by GH treatment. Maternal and fetal metabolic status was significantly affected by maternal food intake. We conclude that maternal GH treatment increases placental transport capacity, but that anabolic effects in the mother may limit fetal substrate supply and therefore prevent an increase in fetal growth.

Animals↗
PubMed2006

Expression profile and protein levels of placental products as indirect measures of placental function in in vitro-derived bovine pregnancies.

Bovine conceptus development and its association with placental proteins present in maternal, foetal and neonatal plasma and foetal (amniotic and allantoic) fluids were investigated in in vivo- and in vitro-produced (IVP) concepti and newborn calves. Females were superovulated to obtain control embryos, whereas IVP embryos were derived from established in vitro procedures. Pregnant animals were slaughtered on days 90 or 180 of gestation or allowed to develop to term for the assessment of physical traits. Foetal, maternal and neonatal blood and foetal fluids were collected for the determination of bovine placental lactogen (bPL) and bovine pregnancy-specific protein B (bPSPB) concentrations. Placental transcripts for bPL and bPSPB, determined by quantitative RT-PCR, were elevated in IVP placentomes. No major physical differences were observed between groups on day 90, but concentrations of bPL and bPSPB were higher in foetal plasma and allantoic fluid of IVP concepti in day 180 pregnancies, which were correlated with larger uterine and conceptus traits. Maternal concentrations of bPL in IVP pregnancies were lower than controls during the last 8 weeks of gestation, to become similar as parturition approached. Newborn IVP calves and foetal membranes were larger and displayed higher concentrations of plasma bPL than controls (10 and 60 min after birth). Our results indicated that differential patterns of secretion of bPL and bPSPB into the maternal and foetal systems occurred at distinct stages of gestation, and these were associated with altered conceptus development after in vitro embryo manipulations, indirectly demonstrating deviations in placental function in IVP pregnancies.

Allantoin↗
PubMed1986

[Value of placental enzymes, endocrinologic parameters of pregnancy and placental perfusion in cases of intrauterine growth retardation].

The serum HCS concentration and urine estriol (E3) content was determined just before delivery in mature but intrauterine retarded and mature eutrophic cases. The hormonal parameters and the placental perfusion index (PPI) were determined in each case parallel. The mitochondrial glutamate dehydrogenase (GLDH) and the glycolytic lactate dehydrogenase (LDH) activity in the placentas were determined immediately after the placentas were born. Among the cases in which intrauterine retarded newborns were born the half of the women had gestosis during their pregnancy and the half had not any problem. It has been found that serum HCS concentration and urine E3 content were significantly lower in the pathologic groups compared to the control. The placental LDH activity significantly increased in both of the dysmature groups. The GLDH activity was normal in the toxemic cases but decreased significantly in the cases where the newborns were dysmature and the mother had no toxemia. There was a correlation between the serum HCS concentration and placental GLDH activity in non-toxemic cases. The perfusion was significantly lower in the toxemic cases only. At the same time there was no correlation between the placental perfusion and endocrine parameters or enzyme activities in both of the pathologic groups.

Estriol↗
PubMed1977

Effect of prostaglandin PGE2alpha on the synthesis of placental proteins and human placental lactogen (HPL).

The biosynthesis of placental proteins and placental lactogen (HPL) was studied in vitro in 10-12 week, 16-18 week and term human placenta in the presence and absence of PGF2alpha. The highest 14C-leucine incorporation was detected in 10 to 12 weeks old placentas of PGF2alpha to the incubation medium depressed the rate of incorporation of 14C-leucine into placental proteins in a dose dependent manner. Placentas most sensitive to this action of PGF2alpha were those obtained at 18 weeks of gestation followed by placentas at term. In vivo application of PGF2alpha for therapeutic induction of abortions resulted in the marked inhibition of placental protein synthesis in vitro.

Abortion, Induced↗
PubMed1995

The effects of maternal aerobic exercise on human placental development: placental volumetric composition and surface areas.

The histomorphometry of term placentae from women who exercised regularly throughout either the first half or all of pregnancy was compared to that of placentae from matched controls to determine if regular exercise during pregnancy produced histomorphometric evidence of altered development and transport capacity. Conventional stereological techniques were used to estimate placental volumetric composition, surface areas, and villous and vascular configurations in the three groups. Exercise confined to early pregnancy increased the parenchymal component of the placenta, total vascular volume and site-specific capillary volume and surface area. Exercise throughout pregnancy increased these and multiple other histomorphometric parameters associated with the rate of placental perfusion and transfer function. However, significant changes were confined to villi > 80 microns in diameter. The localization of both the timing of the stimulus and the anatomical sites affected indicates that regular, sustained exercise modifies placental development primarily in early and mid-pregnancy. We speculate that the lack of significant changes in the structure and configuration of the smaller villi indicates that other adaptive mechanisms, such as increased rates of placental blood flow, must be well developed by the latter portion of the mid-trimester and adequately maintain fetal oxygenation and substrate delivery throughout the third trimester.

Adult↗
PubMed1994

Ca2+ entry through L-type voltage-sensitive Ca2+ channels stimulates the release of human chorionic gonadotrophin and placental lactogen by placental explants.

The release of human chorionic gonadotrophin (hCG) and placental lactogen (hPL) by human placental explants can be stimulated by Ca2+ entry. The aim of the present study was to characterize the modality of Ca2+ entry in the presence of high extracellular K+ concentration ([K+]o). A rise in [K+]o from 5 to > or = 50 mM induced a rapid and marked increase in the release of hCG and hPL from human term placental explants. The stimulatory effects of an excess [K+]o on the release of hCG and hPL were blocked in the absence of extracellular Ca2+ or in the presence of 0.5 mM Co2+. The presence of 50 microM methoxyverapamil, 20 microM nifedipine or 40 microM Cd2+ in the medium inhibited the stimulatory effects of [K+]o addition. Lastly, 40 microM Ni2+ failed to affect the increases in hCG and hPL releases elicited by [K+]o addition. Our data clearly show that a rise in [K+]o stimulates the release of hCG and hPL from placental explants. These secretory effects can be viewed as resulting from a Ca2+ entry through voltage-sensitive Ca2+ channels of the L-type.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

Plasminogen activator of urokinase type and its inhibitor of placental type in hypertensive pregnancies and in intrauterine growth retardation: possible markers of placental function.

OBJECTIVE: Our purpose was to study the plasma concentrations of the plasminogen activator of urokinase type and its specific inhibitor of placental type in pregnancies complicated by hypertension or fetal growth retardation. STUDY DESIGN: Consecutive patients with pregnancy-induced hypertension (n = 17), mild preeclampsia (n = 17), severe preeclampsia (n = 19), and intrauterine growth retardation (n = 19) were studied. Blood samples were obtained just before delivery (mean 2 days). Women with normal pregnancies (n = 40), longitudinally followed between the tenth and fortieth gestational weeks, served as a control group. RESULTS: The plasma concentrations of the urokinase type antigen were significantly lower in women with severe preeclampsia or intrauterine growth retardation than those in women with normal pregnancies (p < 0.001). In all four groups with complicated pregnancies the antigen concentrations of the urokinase type and its inhibitor were significantly correlated with both placental weight and birth weight. CONCLUSIONS: The plasma concentration of the urokinase type antigen would appear to reflect placental function, and both the antigen and its inhibitor concentrations are correlated with placental and fetal growth.

Birth Weight↗
PubMedDate not supplied

Stimulatory effects of extracellular calcium on chorionic gonadotrophin and placental lactogen release by human placental explants.

The effects of sudden modifications of extracellular calcium ion concentration on human chorionic gonadotrophin (hCG) and human placental lactogen (hPL) release were investigated using term placental explants incubated in Krebs Ringer solution. The hCG and hPL releases were both stimulated when the extracellular Ca2+ concentration was increased. The hCG and hPL secretions elicited by the addition of extracellular Ca2+ were larger when placental explants were preincubated in alpha-calcium (no added calcium + EGTA) than in normo-calcium (1.5 mM). Removal of extracellular Ca2+ from the medium also elicited an increase in hCG and hPL release. However, this stimulatory effect of Ca2+ omission was partly suppressed by washing the explants prior to incubation in the alpha-calcium medium, and was completely abolished when alpha-calcium medium was supplemented with 1 mM cobalt. Our results indicate that changes in Ca2+ modify hCG and hPL release from term placental explants in a manner concordant with the 'stimulus-secretion coupling' concept.

Calcium↗
PubMed1994

The release of human chorionic gonadotrophin and placental lactogen by placental explants can be stimulated by Ca2+ entry through a Na(+)-Ca2+ exchange process.

Isosmotical replacement of extracellular Na+ ([Na+]o) by K+, choline and to a lesser extent by saccharose stimulated the release of chorionic gonadotrophin and placental lactogen from human term placental explants. The effect of [Na+]o removal on the release of both hormones was concentration-dependent and was inhibited in the absence of extracellular Ca2+ or in the presence of 0.5 mM Co2+, a Ca2+ entry blocker. Blockers of the voltage-sensitive Ca2+ channels (20 microM nifedipine and 50 microM methoxyverapamil) or Na+ channels (5 microM tetrodotoxin) did not affect the stimulatory effects of [Na+]o omission. By contrast, Mg2+ and Sr2+ (10 mM) as well as amiloride (2 mM) and its analogue 2',4'-dimethylbenzamil (50 microns), all known to affect the Na(+)-Ca2+ exchange, markedly reduced the increase in hormone release elicited by [Na+]o removal. Lastly, the secretory responses to [Na+]o deprivation were increased in the presence of 2 mM ouabain, an inhibitor of the Na(+)-K+ ATPase. These results indicate for the first time that [Na+]o omission provokes a Ca(2+)-dependent stimulation of human chorionic gonadotrophin and placental lactogen releases. The pharmacological dissection of the secretory effects of [Na+]o removal supports the existence of a process of Na(+)-Ca2+ exchange in placental cells.

Calcium↗
PubMed1991

Interaction of human placental ribonuclease with placental ribonuclease inhibitor.

The interactions of human placental ribonuclease inhibitor (PRI) with bovine pancreatic ribonuclease (RNase) A and human angiogenin, a plasma protein that induces blood vessel formation, have been characterized in detail in earlier studies. However, studies on the interaction of PRI with the RNase(s) indigenous to placenta have not been performed previously, nor have any placental RNases been identified. In the present work, the major human placental RNase (PR) was purified to homogeneity by a five-step procedure and was obtained in a yield of 110 micrograms/kg of tissue. The placental content of angiogenin was also examined and was found to be at least 10-fold lower than that of PR. On the basis of its amino acid composition, amino-terminal sequence, and catalytic properties, PR appears to be identical with an RNase previously isolated from eosinophils (eosinophil-derived neurotoxin), liver, and urine. The apparent second-order rate constant of association for the PR.PRI complex, measured by examining the competition between PR and angiogenin for PRI, is 1.9 X 10(8) M-1 s-1. The rate constant for dissociation of the complex, determined by HPLC measurement of the rate of release of PR from its complex with PRI in the presence of a scavenger for free PRI, is 1.8 X 10(-7) s-1. Thus the Ki value for the PR.PRI complex is 9 X 10(-16) M, similar to that obtained with angiogenin, and 40-fold lower than that measured with RNase A. Complex formation causes a small red shift in the protein fluorescence emission spectrum, with no significant change in overall intensity. The fluorescence quantum yield of PR and the Stern-Volmer constant for fluorescence quenching by acrylamide are both high, possibly due to the presence of an unusual posttranslationally modified tryptophan residue at position 7 in the primary sequence.

Amino Acids↗
PubMed2002

Placental-specific IGF-II is a major modulator of placental and fetal growth.

Imprinted genes in mammals are expressed from only one of the parental chromosomes, and are crucial for placental development and fetal growth. The insulin-like growth factor II gene (Igf2) is paternally expressed in the fetus and placenta. Here we show that deletion from the Igf2 gene of a transcript (P0) specifically expressed in the labyrinthine trophoblast of the placenta leads to reduced growth of the placenta, followed several days later by fetal growth restriction. The fetal to placental weight ratio is thus increased in the absence of the P0 transcript. We show that passive permeability for nutrients of the mutant placenta is decreased, but that secondary active placental amino acid transport is initially upregulated, compensating for the decrease in passive permeability. Later the compensation fails and fetal growth restriction ensues. Our study provides experimental evidence for imprinted gene action in the placenta that directly controls the supply of maternal nutrients to the fetus, and supports the genetic conflict theory of imprinting. We propose that the Igf2 gene, and perhaps other imprinted genes, control both the placental supply of, and the genetic demand for, maternal nutrients to the mammalian fetus.

Alleles↗
PubMed1992

Placental-specific expression from the mouse placental lactogen II gene promoter.

The gene for mouse placental lactogen II (mPL-II) has been isolated and characterized. This gene contains five exons, with a transcription start site 59 nucleotides upstream of the translation initiation ATG. Introduction of a DNA construct containing 2.7 kilobases of sequence upstream of the mPL-II transcription initiation site directed the synthesis of a linked coding region for the simian virus 40 large and small tumor antigens in placental trophoblast giant cells of transgenic mice. The pattern of simian virus 40 transgene expression in the placenta was indistinguishable from that of the endogenous mPL-II gene. In contrast, the first 569 base pairs upstream of the transcription start site proved insufficient to direct placental expression. Thus, one or more elements required for placental trophoblast giant cell expression have been localized to a region between -2700 and -569 of the mPL-II gene.

Amino Acid Sequence↗
PubMed1998

Rat placental lactogen II gene: characterization of gene structure and placental-specific expression.

Rat placental lactogen II (rPLII) was the first described member of the rat PRL-like placental gene family in which nine novel proteins have now been identified. In this article, we present data on the isolation and characterization of the rPLII gene. Two genomic clones, GC I (18.5 kb) and GC II (9.4 kb), were isolated from an EMBL3 Sprague-Dawley rat liver genomic DNA library. GC I, which was used for further analysis, contains the entire coding region and extensive 5' and 3' flanking information. The rPLII gene, estimated to be 5.4 kb in size, has the same five-exon and four-intron structure and identical intron/exon splice sites and types as the rPRL gene. A major transcription start site 58 bp upstream of the initiator methionine codon and several minor sites 1-3 bp 5' and 3' of this site were identified by primer extension of day 18 placental messenger RNA. The rPLII gene has been localized to chromosome 17, using a series of hybrid cell lines derived from mouse hepatoma cells (MWTG3) and adult rat hepatocytes; this is the same chromosome designation as the PRL gene itself and other cloned placental members of this gene family. Luciferase reporter constructs containing 5' flanking DNA sequences were tested in transient transfection assays in the rat choriocarcinoma cell line, Rcho, and the rat pituitary GC cell line. Both a 4.5- and 3-kb 5' flanking sequence supported luciferase expression in the Rcho but not the GC cells. A 765-bp fragment showed no activity in either cell type. Transient transgenic mice, generated with the 3-kb 5' rPLII/luciferase construct, expressed varying amounts of luciferase expression in the placenta.

Amino Acid Sequence↗
PubMed1983

Characterization of the synthesis and release of human placental lactogen and human chorionic gonadotropin by an enriched population of dispersed placental cells.

An enriched fraction of human placental cells that synthesize and release both placental lactogen (hPL) and hCG was obtained by isopycnic centrifugation of collagenase/hyaluronidase-dispersed cells through a density gradient of 40% Percoll. The enriched cells, which banded at a density of approximately 1.01 g/ml, comprised 10-15% of the total DNA. During the first 24 h after attachment, the cells released 50-250 ng hPL and 4-10 mIU hCG/10(6) cells. Thereafter, the rate of hPL release decreased, while the rate of hCG and [35S]trichloroacetic acid-precipitable protein release remained constant. The enriched cells responded to phospholipase A2, low extracellular calcium, and (Bu)2cAMP in a manner similar to that of placental explants. Phospholipase A2 (0.1 and 1 U/ml) stimulated hPL release by 270% and 568%, respectively, and low extracellular calcium (0-0.18 mM) stimulated hPL release by 48%. (Bu)2 cAMP (1 mM) stimulated hCG release by 42%, but had no effect on hPL. Estradiol (10(-5)-10(-12) M) and progesterone (10(-5)-10(-10) M) had no effect on the synthesis and release of either hPL or hCG over a 6-day period. In addition, insulin (8.3 X 10(-7) M) and changes in medium glucose content (0-5 mg/ml) had no effect on hPL release over a 72-h period. Since the enriched trophoblast cells respond to provocative stimuli in a manner similar to that of explants and placental fragments, this cell population is a useful model system for investigations of the cellular mechanisms of hPL and hCG release.

Bucladesine↗
PubMed1990

Human placental lactogenic hormone as a parameter for placental function in renal transplanted women.

In 13 pregnant women with renal transplants the serum concentration of placental hormones were determined in order to show their ability to predict fetal problems especially placental insufficiency. It is shown that the hPL values were increased because of reduced elimination of hPL, presumably in the renal tubuli. In this study the weight of only one newborn was over the 50th percentile in spite of the fact that all but one had hPL values over the 50th percentile and in even 8 pregnancies the values were over the 95th percentile. In most of the growth-retarded fetus's the ratio between hPL and the weight of the newborns was more complex. It is concluded that in renal transplanted pregnant women, hPL as a parameter for the placental function must be used with reservation and is not able to predict placental insufficiency.

Azathioprine↗
PubMed1985

Arachidonic acid stimulates phosphoinositide hydrolysis and human placental lactogen release in an enriched fraction of placental cells.

Previous investigations in this laboratory have indicated that arachidonic acid stimulates a rapid, dose-dependent, and reversible increase in human placental lactogen (hPL) release which is not dependent on cyclooxygenase or lipoxygenase metabolism. To investigate further the mechanism by which arachidonic acid stimulates the release of hPL, the effects of arachidonic acid on phosphoinositide hydrolysis were examined in an enriched cell culture population of term human syncytiotrophoblast. Phosphoinositide hydrolysis was assayed by three methods: the release of 3H from perfused cells prelabeled with [3H]myoinositol, the measurement of inositol phosphate accumulation, and the distribution of radioactivity in phospholipids separated by two-dimensional thin layer chromatography after exposure of 32P-labeled placental cells to arachidonic acid. Arachidonic acid stimulated a concentration-dependent, rapid, and reversible increase in the release of both [3H]myoinositol and hPL from perfused placental cells. This effect was not inhibited by prior incubation of cells with indomethacin (20 microM). In contrast, palmitic acid and oleic acid stimulated phosphoinositide hydrolysis only at a high concentration (100 microM). Arachidonic acid also stimulated the rapid appearance of inositol monophosphate in placental cells. The effect of arachidonic acid was specific for hydrolysis of phosphoinositides and phosphatidylserine and did not involve other phospholipids. Since phosphoinositide hydrolysis is associated with hormone release in a variety of secretory systems, these results suggest that the stimulation of hPL release by arachidonic acid may be mediated, at least in part, by the activation of phospholipase C.

Arachidonic Acid↗
PubMed1985

In vivo and in vitro studies on the production of placental proteins (human chorionic gonadotropin, human placental lactogen, and pregnancy-specific beta 1-glycoprotein) in an adrenal choriocarcinoma.

The ectopic production of placental proteins (human chorionic gonadotropin [hCG], human placental lactogen, and pregnancy-specific beta 1-glycoprotein) by an adrenal choriocarcinoma was investigated experimentally in vivo and in vitro. By an immunohistochemical method, the choriocarcinoma tissues obtained from the right adrenalectomy were found to react with hCG, human placental lactogen, and pregnancy-specific beta 1-glycoprotein antibodies. The concentrations of hCG-beta, human placental lactogen, and pregnancy-specific beta 1-glycoprotein in the tumor fluid were 1480, 100, and 47 ng/mL, respectively. On incubation of the tumor slices in vitro, the concentration of hCG-beta in the incubation medium increased markedly with time. Serial sections of the removed uterus and right ovary did not reveal any primary trophoblastic lesions. The present tumor responded well to double chemotherapy with actinomycin D and methotrexate, resulting in a decrease of the level of serum hCG-beta to less than 10 ng/mL after four courses of the chemotherapy.

Adrenal Gland Neoplasms↗