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At least 811 records · Page 45Linked to original sources
PubMed2000

Functional heterodimerization of prolactin and growth hormone receptors by ovine placental lactogen.

Although homo- or heterodimerization are common mechanisms for activation of cytokine receptors, cross-talk between two distinct receptors in this superfamily has been never shown. Here we show a physiologically relevant example indicating that such an interaction does occurs, thus raising the hypothesis that heterodimerization between distinct cytokine receptors may be a novel mechanism contributing to the diversity of cytokine signaling. These findings were documented using both surface plasmon resonance and gel filtration experiments and show that ovine placental lactogen (PL) heterodimerizes the extracellular domains (ECDs) of ruminant growth hormone receptor (GHR) and prolactin receptor (PRLR). We also show that PL or PL analogues that exhibit little or no activity in cells transfected with PRLRs and no activity in cells transfected with ovine GHRs exhibit largely enhanced activity in cells cotransfected with both PRLRs and GHRs. Furthermore, chimeric receptors consisting of cytosolic and transmembrane part of ovine GHR or ovine PRLR and ECDs of human granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) alpha or beta were constructed. Upon transfection into Chinese hamster ovary cells along with reporter luciferase gene and stimulation by GM-CSF, a significant increase in luciferase activity occurred when GM-CSFR-alpha-PRLR and GM-CSFR-beta-GHR or GM-CSFR-alpha-GHR and GM-CSRR-beta-PRLR were cotransfected. In conclusion, we show that ovine PL is capable of functional heterodimerization of GHR and PRLR and that when their cytosolic parts, coupled to the ECD of GM-CSF receptors, are heterodimerized by GM-CSF, they are capable of transducing biological signal.

Animals↗
PubMed1998

Nucleotide sequence analyses predict that human pituitary and human placental gonadotropin-releasing hormone receptors have identical primary structures.

Gonadotropin-releasing hormone (GnRH) interacts with a putative receptor in human placenta to cause the dose-dependent release of human chorionic gonadotropin (hCG) in a manner analogous to hypothalamic GnRH stimulation of luteinizing hormone (LH), and follicle-stimulating hormone (FSH) by the pituitary gland. However, GnRH agonists bind a placental binding site at a lower affinity than they bind the pituitary GnRH receptor, suggesting the two sites differ. To address this issue, human placental GnRH receptor mRNA from an 8-wk placental sample was amplified using primers based on the sequence of the human pituitary receptor, cloned, and sequenced. The sequence of the placental transcript was found to be identical to its pituitary counterpart. Thus, as with the pituitary receptor, this placental receptor transcript appears to encode a single polypeptide chain with seven intramembranous domains and two glycosylation sites. However, it is possible these receptors differ in their posttranslational processing or there is more than one placental GnRH receptor. In addition, subsequent gene amplification studies, modified to increase the sensitivity of the method, revealed a band of the predicted size (approximately 1051 bp) in a 6-wk and two 8-wk placental samples, but not in 5-wk and 7-wk samples. The failure to amplify GnRH receptor mRNA at these gestational ages did not appear to be an issue of cell health or sample degradation, since GnRH, alpha hCG, and beta hCG mRNA were amplified from each of these tissues. Instead these data suggest GnRH receptor mRNA may have a short half-life or the mRNA may be translated as rapidly as it is transcribed, with the result that it has not accumulated in the cell.

Amino Acid Sequence↗
PubMed1986

Inhibition of binding of ovine placental lactogen to growth hormone and prolactin receptors by monoclonal antibodies.

From a single cell fusion, five stable hybridomas secreting antiovine placental lactogen (oPL) antibodies were obtained. Three of these secrete immunoglobulin (Ig)G subclass, and the other two secrete IgM class antibodies. Ascites fluids were raised in mice for each clone and were used as the antibody component for the development of solid phase RIA. Three solid-phase RIAs were successfully established using individual IgG subclass monoclonal antibodies, but the IgM class antibodies were ineffective. In all three individual solid-phase RIAs, the binding of [125I]iodo-oPL to the immobilized antibody was inhibited by unlabeled oPL, but not by ovine pituitary PRL (oPRL), ovine GH (oGH), or ovine pituitary extract. Two of the IgG subclass antibodies were able to inhibit the binding of [125I] iodo-oPL to PRL receptors(s) and to GH receptor(s) in rabbit mammary gland and liver, respectively. One of these two IgG subclass antibodies was more effective at inhibiting the binding of oPL to PRL receptor(s) in rabbit mammary gland, whereas the other one is more effective in inhibiting the binding of oPL to GH receptor(s) in rabbit liver. These antibodies, however, could only weakly inhibit the binding of [125I]iodo-oPRL to rabbit mammary gland and were ineffective in inhibiting the binding of [125I]iodo-oGH to rabbit liver. The addition of monoclonal antibodies in both radioreceptor assay (RRA) for PRL (RRA-PRL) and for GH (RRA-GH) did not affect the parallelism of the displacement curve of oPL standard. Our results suggest that oPL might contain two distinct binding sequence(s): one responsible for the binding of oPL to PRL receptor(s) and the other responsible for the binding of oPL to GH receptor(s). These two binding sequences might overlap or be located adjacent to one another. The interaction of monoclonal antibodies with these binding sequences of oPL may block the binding of oPL with PRL and GH receptor(s). Alternatively, our studies suggest that the monoclonal antibodies do not bind to hormone receptor(s)-binding sequence(s) in oPL, but the interaction between oPL and monoclonal antibody might alter the conformational structure of the oPL which will consequently lead to a lower binding of oPL to PRL and GH receptor(s).

Animals↗
PubMed1982

Chromosomal localization of the human placental lactogen-growth hormone gene cluster to 17q22-24.

Recombinant plasmid HCS-pBR322 containing a 550-base-pair (bp) insert of cDNA to human placental lactogen (hPL) mRNA was 3H-labeled by nick translation and hybridized in situ to human chromosome preparations in the presence of 10% dextran sulfate. A high percentage of cells (80%) were found to exhibit label on the distal end of the long arm of chromosome 17. Silver grains on this region constituted 25.5% of all labeled sites, allowing assignment of the hPL and growth hormone (hGH) genes, which have over 90% nucleotide homology in their coding sequences, to 17q22-24. A gene copy number experiment showed that both genes are present in approximately three copies per haploid genome.

Chromosome Banding↗
PubMed1993

Syncytiotrophoblastic localization of the human growth hormone variant mRNA in the placenta.

The hGH/hCS genes, clustered on chromosome 17 in the 5' to 3' order GH-N, CS-L, CS-A, GH-V and CS-B, show a high degree of sequence identity. The expression product of the GH-V gene is the placental growth hormone, which replaces pituitary GH in maternal blood throughout pregnancy. By means of mRNA competitive hybridization using 32P-labelled and unlabelled 30 bases long oligonucleotides, we first optimized specific hybridization conditions. In situ hybridization was then performed to locate the GH-V mRNA encoding placental growth hormone. The hGH-V gene appears expressed in the placental syncytiotrophoblast. Unlike the CS-A and CS-B genes (both encoding hPL) which are expressed uniformly in the syncytiotrophoblast, the GH-V mRNA is located in a few syncytiotrophoblast cells only.

Base Sequence↗
PubMed1993

Effect of 1-34 human parathyroid hormone upon first trimester placental human chorionic gonadotrophin secretion in vitro: potentiation by epidermal growth factor.

Human chorionic gonadotrophin (HCG) secretion by the early placenta is under multifactorial control. Epidermal growth factor (EGF) has been reported to be involved in regulating the formation and secretion of HCG by first trimester placental explants in culture. The effect of the amino-terminal fragment of parathyroid hormone (1-34 PTH), a calciotrophic factor upon HCG secretion, and its possible interaction with EGF were examined in this study, both in static cultures and in superfusion, where it has previously been demonstrated that HCG secretion is spontaneously pulsatile. Gestational age-dependent effects of 1-34 PTH were noted in both models. In static cultures, 1-34 PTH stimulated HCG secretion in 7-9 week placenta, in a biphasic fashion, the maximal effect being noted at 10-25 ng/ml concentrations (250-270%), while at 1 and 100 ng/ml, the effect was mild. In superfusion, the effect of 1-34 PTH added overnight was also stimulatory, as shown by the significantly increased pulse amplitude and area under the curve. Effects of 1-34 PTH at 11-14 weeks were inhibitory. In static cultures at 7-9 weeks, the stimulatory effect of 25 ng 1-34 PTH was increased by 70% when EGF (100 ng/ml) was added. However at 11-14 weeks, this combined effect was inhibitory. We conclude that 1-34 PTH has an endocrine effect on secretion of HCG by the first trimester placental tissue, and this effect is potentiated by the addition of EGF.

Chorionic Gonadotropin↗
PubMed1981

Endocrine balance as a factor in the etiology of the fetal alcohol syndrome.

It is well documented that children with the fetal alcohol syndrome are a direct consequence of heavy maternal ethanol consumption during pregnancy. The mechanism by which ethanol exerts its teratogenic effect is however, far from understood. Recent experimental evidence has shown alcohol to have a direct inhibitory effect on embryogenesis. Little information, however, is available concerning other factors associated with maternal drinking which may contribute to abnormal fetal development. Proper materno-fetal hormonal balance is essential to insure successful pregnancy outcome. Of particular importance with respect to normal fetal development, are the levels of placental tropic hormones; pituitary hormones such as prolactin and oxytocin; adrenal cortical hormones; both maternal and fetal thyroid hormones; maternal and fetal sex hormones; and maternal insulin. Ethanol alters the levels of a variety of hormones associated with the hypothalamic/pituitary-gonadal, -adrenal and -thyroid axes. Many of these alterations have been observed in the male, however, with little data available on the female. In spite of the known adverse effect of ethanol on certain aspects of female reproductive function, few if any studies have examined the effects of alcohol ingestion during pregnancy on maternal endocrine balance. It is hoped that the present review will provide a rationale for the examination of alcohol effects on maternal endocrine hormones, as well as to provide possible target areas with respect to fetal development subsequent to ethanol-induced endocrine imbalance.

Alcoholic Beverages↗
PubMed2001

Mechanisms regulating angiotensin II responsiveness by the uteroplacental circulation.

Pregnancy is associated with increases in cardiac output and uterine blood flow (UBF) and a fall in systemic vascular resistance. In ovine pregnancy, UBF rises from approximately 3% of cardiac output to approximately 25% at term gestation, reflecting a >30-fold rise in UBF by term. This increase in UBF supports exponential fetal growth during the last trimester and maintains fetal well-being by providing excess oxygen and nutrient delivery. These hemodynamic changes are associated with numerous hormonal changes, including increases in placental steroid hormones and enhanced activation of the renin-angiotensin and sympathetic nervous systems, all of which are believed to modulate systemic and uterine vascular adaptation and vascular reactivity. Systemic pressor responses to infused ANG II are attenuated in normotensive pregnancies and the uteroplacental vasculature is even less sensitive, suggesting development of mechanisms to maintain basal UBF and permit the rise in UBF necessary for fetal growth and well-being. The effects of ANG II on the uteroplacental vasculature are reviewed, and the mechanisms that may account for attenuated vascular sensitivity are examined, including ANG II metabolism, vascular production of antagonists, ANG II-receptor subtype expression, and the role of indirect mechanisms.

Angiotensin II↗
PubMed1988

Inhibition of human placental microsomal aromatase by thyroid hormone and iodothyronine derivatives.

The initial velocity kinetics of the effect of thyroid hormone and analogs on human placental microsomal aromatase were studied. Thyroxine and its propionic analog 3,5,3',5'-tetraiodothyropropionic acid show a competitive inhibition with an apparent Ki of 1.4 microM and 8.5 microM, respectively, towards androstenedione aromatization. 3,5,3'-Triiodothyronine with a Ki of 1.8 microM shows a decreased affinity compared to thyroxine. Two analogs, 3,5,3'-triiodothyropropionic acid and 3,5,3'-triiodothyroacetic acid appear to have negligible competition.

Aromatase Inhibitors↗
PubMed1998

Thyroid function in early pregnancy. II: Paradoxical growth hormone response to thyrotropin-releasing hormone.

A variant of growth hormone (GH) known as human placental growth hormone (hpGH) is found in maternal serum during pregnancy. It is well established that during the second half of normal pregnancy, pituitary GH secretion is suppressed; however, there are no data about maternal GH secretion during the first trimester of pregnancy. The present study reports the response of GH to thyrotropin-releasing hormone (TRH) in eight pregnant women in the trimester of pregnancy (weeks 6-9) who had previously requested voluntary interruption of pregnancy. The TRH test induced a significant paradoxical GH response with a peak of 9.4 +/- 0.5 ng/ml (mean +/- SD) at 30 min and a higher thyroid-stimulating hormone (TSH) response in pregnant women. The increment was observed until 120 min and no response was observed in the control group. These data show the paradoxical response of GH to TRH, a releasing factor to which the hormone does not normally respond. This paradoxical secretion may be due to direct pituitary stimulation and can be explained on the basis of a state of gestational hypothyroidism.

Adolescent↗
PubMed1980

[Changes in obstetric management over the past decade (author's transl)].

Over a observation period of 10 years (1969-1979) developments in perinatal control techniques, mostly started in the 1st Department of Obstetrics and Gynaecology, University of Vienna, at the beginning of that period, and their effect on the obstetric management are presented. In contrast to a trend of decreasing birth rate for the whole of Austria the annual numbers of deliveries in this hospital remained -after a temporary increase-unchanged. Subpartial cardiotocographic monitoring is presently applied in about 95% of all cases. The frequency of Caesarean sections has risen from below 4% to approximately 8% over the past years. Simultaneously, a shift was observed from vital to preventive fetal indications in Caesarean sections, with a parallel tendency to relatively fewer vaginal-operative deliveries. The uncorrected perinatal mortality rate has been lowered to 1.35%. This decrease is partly due to our efforts to select high-risk pregnancies in order to control them intensively. Thus, ultrasound examinations have been liberally put into practice, e.g. leading to an early diagnosis of multiple pregnancy. Use of tocolytic drugs, as well as surgical closure of the cervix together with intensive prenatal care of pregnant women with a high risk of prematurity have proved their worth as compared with control groups. Due to early and special interest in research and in monitoring of placental insufficiency, hormone determinations and measurements of placental perfusion by isotopes took a fixed place in monitoring of high-risk pregnancies early on during the observation period. Evaluation of fetal lung maturity by amniocentesis now enables us to make well-grounded decisions to stop tocolytic measures or to induce labour. In the latter field the local application of prostaglandins to the cervix by an adaptor has recently opened up new aspects. Attention has also been paid to the emotional aspect by new techniques of psychprophylactic preparation for childbirth and by a policy of rooming-in of mother and child.

Cesarean Section↗
PubMed1997

Placental progonadotropin-releasing hormone (pro-GnRH) in the rhesus monkey.

Gonadotropin-releasing hormone (GnRH) has been shown to play a role in the regulation of human chorionic gonadotropin (hCG) secretion by the human placenta. Molecular studies have demonstrated that human placental trophoblast cells synthesize a progonadotropin-releasing hormone (pro-GnRH) identical to its human hypothalamic counterpart. However, far less is known about nonhuman primates. To determine whether pro-GnRH exists in the rhesus placenta, pro-GnRH mRNA was cloned, sequenced, and shown to be 97.6% homologous to its human placental counterpart. A single base difference (base 1167) in the domain encoding GnRH results in the same amino acid, arginine, in position 8, whereas four base differences (bases 1200, 1253, 1268, 1292) in the domain encoding GnRH-associated peptide (GAP) result in four different amino acids in position 19, 37, 42, and 50. The absence of a basic amino acid in position 50 suggests the rhesus sequence may be cleaved to yield GAP peptides different from the human placenta. Thus, these data justify the use of mammalian GnRH in studies of rhesus placental function, but indicate the need to investigate the roles unique GAP peptides may play in placental/uterine function.

Amino Acid Sequence↗
PubMed1994

Placental lactogen and somatotropin: hormone binding to the corpus luteum and effects on the growth and functions of the ovary in heifers.

The effects of recombinant bovine placental lactogen (rbPL) and recombinant bovine somatotropin (rbST) on development of ovarian follicles and CL were tested in heifers. Estrus (day = 0) was synchronized and heifers were treated (Days 0-21) with either saline (control; n = 7), rbST (25 mg/day; n = 6), or rbPL. (50 mg/day; n = 8). Blood was collected daily for analyses of progesterone, estradiol, ST, PL, and insulin-like growth factor (IGF)-I; ultrasound was performed daily for measurement of follicles and CL. PL in plasma (mean +/- SE; ng/ml) averaged 4.1 +/- 0.2 for rbPL-treated heifers, and ST in plasma (ng/ml) averaged 2.7 +/- 0.3 for rbST-treated heifers. IGF-I in plasma (ng/ml) was increased for rbST-treated (198 +/- 10; p < 0.001) and rbPL-treated (143 +/- 9; p < 0.06) heifers compared to controls (117 +/- 9). After Day 9 of the estrous cycle, heifers treated with rbPL had larger CL (p < 0.001) and more progesterone in plasma (p < 0.001) than controls, whereas rbST-treated heifers were intermediate for these measures. Largest follicles were decreased in size (mm) throughout the estrous cycle for rbPL-treated heifers (12.9 +/- 0.4) compared to controls (14.2 +/- 0.5; p < 0.06) or heifers given rbST (14.0 +/- 0.5; p < 0.11). After Day 17 (preovulatory period), concentrations of estradiol in serum (pg/ml) were decreased for rbST-treated (2.7 +/- 0.3; p < 0.01) and rbPL-treated (2.9 +/- 0.2; p < 0.02) heifers compared to controls (3.8 +/- 0.3).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗