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Results for “PLACENTAL HORMONES”

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At least 541 records · Page 30Linked to original sources
PubMed1993

In vitro effect of anticardiolipin autoantibodies upon total and pulsatile placental hCG secretion during early pregnancy.

BACKGROUND: The anticardiolipin syndrome is characterized among other features by recurrent thromboembolic events, thrombocytopenia, and recurrent fetal loss associated with high IgG titers of anticardiolipin antibodies and/or the presence of lupus anticoagulant. AIMS: The mechanisms for the fetal loss in this syndrome have not yet been clearly elucidated, although several hypothesis based on experimental data have been put forward. We wanted to evaluated the effect in vitro of anticardiolipin antibodies on the secretion of human chorionic gonadotropin. METHODS: Employing our previous experience with placental explants, we studied the effect of several mouse monoclonal and human polyclonal purified anticardiolipin antibodies (ACA), which were shown by us to induce experimental antiphospholipid syndrome (APLS), to affect the pulsatile secretion of beta human choriogonadotropin. RESULTS: The mouse monoclonal ACA antibodies caused an increase in the pulsatility of beta human choriogonadotropin, while human polyclonal ACA derived from patients with ACA had an inhibitory effect. CONCLUSIONS: These studies with placental explants show that ACA may have an additional effect on placental hormone secretion and thus affect the fate of the embryo.

Abortion, Habitual↗
PubMed1994

Fetal hypopituitarism: perinatal endocrine and morphological studies in two cases.

We report two infants with congenital absence of the anterior pituitary gland, documented by magnetic resonance imaging (MRI) or autopsy. In cord plasma obtained at birth from both infants, prolactin (PRL), pituitary growth hormone (hGH), placental growth hormone (hPGH) and thyrotropin (TSH) were undetectable; cortisol was low; thyroxine (T4) was 31 nmol/l in one infant and 85 nmol/l in the other infant who had been treated prenatally with intra-amniotic L-T4 administration. In maternal plasma at birth, PRL, hPGH and T4 were normal and hGH was undetectable. These observations suggest that plasma hGH and PRL in the fetus are exclusively of fetal pituitary origin, hPGH is secreted into the maternal circulation and is not transferred to the fetus and fetal growth can be normal in the absence of hGH, hPGH and PRL in fetal plasma.

Female↗
PubMed1975

Separation of the placenta in the ewe: an ultrastructural study.

Placental separation in the ewe appears to involve an explosive degeneration of the chorionic epithelium which occurs in the short space of time between parturition and the delivery of the fetal membranes. In the goat there is a similar mechanism of separation. By contrast separation of the placenta in the cow appears to depend upon a detachment at the junctional region between fetal and maternal epithelia. There is no obvious explanation for these findings. The results are discussed in the light of the placental hormonal environment in the period which immediately precedes parturition.

Animals↗
PubMed1991

Human immunodeficiency virus type 1 infection of human placenta: potential route for fetal infection.

To determine the potential role of the placenta in transmission of human immunodeficiency virus (HIV) from mother to fetus, the ability of human placental tissue to support HIV type 1 (HIV-1) infection was examined. HIV-1-seronegative first-trimester placentas were maintained in culture and infected with HIV-1. Virus production, measured by HIV-1 antigen release into the supernatant, and HIV-1 DNA, identified by polymerase chain reaction, were detected for at least 12 days postinfection. Western immunoblot analysis showed Gag proteins, precursor p55, and cleavage products p24 and p17 in HIV-1-infected tissues. Double labeling of placental villi with antibodies to CD4 and placental trophoblast-specific alkaline phosphatase indicated that trophoblasts express CD4 antigen. Additionally, immunostaining of HIV-1-infected tissues with anti-p24 antibodies demonstrated HIV-1 protein expression in placental trophoblasts. Evaluation of human chorionic gonadotropin and progesterone production by the placental cultures indicated that there was a 90% decrease in human chorionic gonadotropin and a 70% decrease in progesterone production in HIV-1-infected cultures in comparison with controls. These data demonstrate that trophoblastic cells of human placenta tissue express CD4 and are susceptible to HIV-1 infection; also, placental endocrine function is decreased by HIV-1 infection. Thus, the placenta may serve as a reservoir of HIV-1 infection during pregnancy contributing to infection of the fetus, and decreased placental hormone production may result in impaired fetal development.

Blotting, Western↗
PubMed1987

trans-acting factors interact with a cyclic AMP response element to modulate expression of the human gonadotropin alpha gene.

The alpha subunit of the placental hormone chorionic gonadotropin is regulated by cyclic AMP (cAMP) at the transcriptional level. A cAMP-responsive fusion gene (alpha-CAT) containing 1.5 kilobases of the alpha gene 5'-flanking sequence linked to the chloramphenicol acetyltransferase (CAT) gene was used as a transcriptional reporter in competition assays in transfected JEG-3 choriocarcinoma cells. Expression of the alpha-CAT fusion gene increased linearly with increasing amounts of transfected plasmid and was maximal at the same amount of alpha-CAT DNA (2 micrograms) with or without cAMP treatment. Various amounts of different competitor DNA sequences were cotransfected with the alpha-CAT reporter plasmid to examine the interactions of intracellular trans-acting factors with the regulatory elements of the alpha gene promoter. An 800-base-pair fragment of alpha gene 5'-flanking sequence inhibited both basal and cAMP-stimulated transcription of the alpha-CAT reporter plasmid in a dose-dependent manner, indicative of interactions with one or more trans-acting factors that activate alpha gene expression. The alpha gene sequences that interact with intracellular regulatory factors were defined by using several discrete regions of the 5'-flanking sequence as competitors for alpha-CAT expression. A proximal promoter sequence (-99 to +44) containing the CCAAT box, TATA box, and transcriptional initiation site was a relatively ineffective competitor of alpha-CAT transcription. In contrast, an upstream sequence between -236 and -100 was an effective competitor for transcriptional activators of alpha-CAT expression. Competition for alpha-CAT expression by this regulatory sequence did not require cis interactions with downstream promoter elements and was equally effective with or without cAMP treatment. An 18-base-pair repeated sequence within this region of the alpha gene (-146 to -111) greatly enhanced both basal gene expression and cAMP responsivity and also competed for limiting cellular transcription factors. These findings suggest that JEG-3 cells contain trans-acting factors that interact with a cAMP response element to activate alpha gene transcription. The chorionic gonadotropin beta gene 5'-flanking sequence also competed for alpha-CAT expression, suggesting that a common trans-acting factor is shared by the regulatory sequences of the alpha and beta genes.

Choriocarcinoma↗
PubMed2006

Maternal obesity, metabolism, and pregnancy outcomes.

About one third of all pregnant women in the United States are obese. Maternal obesity at conception alters gestational metabolic adjustments and affects placental, embryonic, and fetal growth and development. Neural tube defects and other developmental anomalies are more common in infants born to obese women; these defects have been linked to poor glycemic control. Preeclampsia, a gestational disorder occurring more frequently in obese women, appears to be due to a subclinical inflammatory state that impairs early placentation and development of its blood supply. Fetal growth and development during the last half of pregnancy depends on maternal metabolic adjustments dictated by placental hormones and the subsequent oxygen and nutrient supply. Maternal obesity affects these metabolic adjustments as well. Basal metabolic rates are significantly higher in obese women, and maternal fat gain is lower, possibly in response to altered leptin function. The usual increase in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing marked postprandial increases in glucose, lipids, and amino acids and excessive fetal exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease postnatally. Impaired glucose tolerance, gestational diabetes, and hyperlipidemia are more common among obese mothers. To date, little attention has been given to the role of diet among obese women in preventing these problems. However, studies of women with impaired glucose tolerance show that replacing refined carbohydrates and saturated fat with complex, low-glycemic carbohydrates and polyunsaturated fatty acids improves metabolic homeostasis and pregnancy outcomes. Thus, current dietary guidelines regarding the amount and type of carbohydrates and fat for nonpregnant women seem appropriate for pregnant women as well.

Adult↗
PubMed1991

Neuropeptides and neurotransmitters in human placental villi.

The human placenta contains many kinds of bioactive substances which are more or less similar to those from the hypothalamic-pituitary-gonadal axis. Most of the studies were carried out mainly with term placenta. The present study, therefore, was attempted to identify, quantify and characterize these substances in the human placenta at the early pregnancy. Using the RIA, immunohistochemistry, HPLC, tissue culture and intrauterine injection methods, we have found that: (1) many kinds of neuropeptides and neurotransmitters are present in the placental villi; (2) LH-RH, NT and SRIF positive immunoreactive granules are localized in the cytotrophoblast and those of beta-EP, 5-HT positive granules in the syncytiotrophoblast; (3) synthetic LH-RH and dynorphin (Dyn) stimulate the hCG secretion of the early placental villi in vitro, and (4) the antisera of LH-RH, NT, Dyn and NE antagonist-alpha-MPT significantly reduced the number of blastocyst implantations in the early pregnant rat. These results indicate that in the human placenta there possibly exists a self-regulation mechanism for the synthesis and secretion of placental hormones and neurotransmitters. Therefore, the human placenta can be regarded as a neuroendocrine organ.

Animals↗
PubMed1983

Relation between pregnancy-associated plasma protein A and fetal sex and blood group.

Maternal pregnancy-associated plasma protein A (PAPP-A) concentration was estimated in 272 pregnancies. Paired samples at 34 weeks of gestation and within 48 h before delivery were compared in relation to fetal and maternal blood group and fetal sex. The PAPP-A values were significantly higher both at 34 weeks and near delivery in rhesus-negative bearers. Mothers of male babies had higher PAPP-A values near delivery but not significantly higher at 34 weeks. This supports earlier findings that some placental hormones are higher in male bearers.

ABO Blood-Group System↗
PubMed1982

Improved in vitro bioassay of follitropin.

The FSH-dependent aromatase activity of Sertoli cell enriched cultures of testicular cells from immature rats was utilized as a sensitive and specific in vitro bioassay for FSH activity. The conversion of 19-hydroxyandrostenedione to estradiol was used as the end point of the assay. By the introduction of a phosphodiesterase inhibitor into the culture medium, the sensitivity was improved 5-10 times, so that 0.05 mIU of FSH showed a response significantly different from the blank. Other pituitary or placental hormones, such as hLH, hTSH and hCG exhibited less than 0.8% cross-reactivity, whereas hGH, hPRL, ACTH1-24, LH-RH, and prostaglandin E2 alpha did not show any cross-reaction at the doses tested.

Animals↗
PubMed1994

Regulation of intrauterine growth: the role of maternal health.

Plasma substrate regulation is outlined in healthy mothers and compared with changes observed in diabetes. Placental exchange of glucose, amino acids and lipids are briefly outlined and regulation by maternal and placental hormones discussed. Fetal adaptation to excess and reduced nutrient supply are shown and fetal hormonal responses described. Examples of how maternal health can affect the offspring in postnatal life are given.

Amino Acids↗
PubMed1997

Prenatal factors influencing long-term outcome.

Animal studies have shown that undernutrition before birth programmes persisting changes in a range of metabolic, physiological and structural parameters. Studies in humans have shown that men and women who had birth weights at the lower end of the normal range, who were thin or short at birth, or who were small in relation to placental size, have increased rates of coronary heart disease. This article suggests how fetal undernutrition at different stages of gestation may be linked to these patterns of early growth. Adaptations by the fetus to undernutrition are associated with changes in the concentrations of fetal placental hormones. Persisting changes in the level of hormone secretion and tissue sensitivity may link fetal undernutrition with adult disease.

Adult↗
PubMed1986

Synthesis of placental proteins by the human placenta perfused in vitro. Preliminary report.

Fresh human placental tissue from deliveries at term was perfused in closed circulation on both the maternal and fetal side. At given times during the 4-hour perfusion period, the amount of human chorionic gonadotropin, human placental lactogen, pregnancy-specific beta 1-glycoprotein and pregnancy-associated plasma protein A was determined in the perfusing buffer. These placental proteins were also quantified in the placental tissue before and after perfusion. Calculations showed that all placentae (n = 3) were able to synthesize all 4 proteins tested.

Chorionic Gonadotropin↗
PubMed1986

Serum bile acids, gamma-glutamyltransferase and routine liver function tests in emetic and nonemetic pregnancies.

The etiology of nausea and vomiting in pregnancy is still unknown. One possibility is that ovarian and placental hormones may play some part. The liver is the major site of metabolic inactivation of steroid hormones. In this study, 102 healthy pregnant women, of whom 62 complained of nausea, were followed throughout pregnancy. Liver function tests were performed to ascertain whether emesis gravidarum is related to impaired hepatic function. In this series, all values were within the normal ranges. Serum levels of total bilirubin and gamma-glutamyl-transferase were significantly decreased and those of total serum bile acids significantly increased in emetic women compared to nonemetic subjects. Furthermore, the metabolic load on the liver seems to follow a biphasic course as there is an apparent minimum in liver function variables in the second trimester. It is concluded that a slow adaptation to the increased hormonal load on the liver might be responsible for the condition of emesis gravidarum.

Adult↗