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PubMed1988

Guanine nucleotide binding in human placental syncytiotrophoblast membranes and comparative regulation of adenylate cyclase in syncytiotrophoblast, turkey erythrocyte and bovine calf testes membranes by guanosine-5'-triphosphate.

Guanosine-5'-triphosphate (GTP) binds specifically to syncytiotrophoblast plasma membranes and increases the production of cyclic AMP in these membranes. 1. In syncytiotrophoblast membranes, GTP alone caused a significant increase in the basal levels of cyclic AMP in a dose dependent manner. 2. GTP alone did not significantly stimulate cyclic AMP production in turkey erythrocyte or bovine calf testes membranes. 3. GTP decreased Gpp(NH)p-mediated cyclic AMP production while increasing NaF-mediated cyclic AMP production in placental, erythrocyte and testes membranes. 4. Since cyclic AMP has been reported to regulate the levels of placental hormones, and it is shown in this study that GTP increases cyclic AMP production in the placenta, this study suggests: (A) placental GTP levels may indirectly regulate placental hormone production, (B) placental beta adrenergic (BA) mediated adenylate cyclase activity may not be regulated in the same manner as the BA system of avian erythrocytes.

Adenylyl Cyclases↗
PubMed1996

Placental steroid hormone synthesis: unique features and unanswered questions.

Despite the amazing diversity of placental architecture across species, a number of common elements can be found, including the ability of all placentae to synthesize and metabolize steroid hormones; the assignment of steroidogenic activities to specific trophoblast phenotypes; the use of novel mechanisms to control expression of steroidogenic enzyme genes, which differ from those employed in the adrenal cortex and gonads; and interactions with the maternal and fetal compartments encompassing supply of steroid hormone precursors as well as regulatory influences of maternal ovarian and pituitary hormones and fetal adrenal cortical steroids.

Animals↗
PubMed1987

Placental-derived mitogenic factor for human fetal adrenocortical cell cultures.

The human fetal adrenal cortex is one of the largest fetal organs and synthesizes precursors for placental estrogen production as part of the feto-placental unit. The factors controlling the rapid growth of the human fetal adrenal cortex during the second and third trimesters are not known. Placental regulation of the growth of human fetal adrenocortical cell cultures from second trimester fetuses was studied. A placental-derived mitogenic factor (PDMF) was detected in tissue homogenates of 14 to 22 week human placentas and stimulated adrenocortical cell number and [3H]thymidine incorporation into DNA 5-8 fold. PDMF has been partially purified by ammonium sulfate precipitation and anion exchange chromatography. PDMF is a heat sensitive protein with disulfide bonds required for activity. The growth stimulation by PDMF was significantly greater than that for basic or acidic fibroblast growth factor by 25-50% and epidermal growth factor by 3-4 fold. The placental hormones, progesterone, estriol, estradiol, placental lactogen and chorionic gonadotropin, either alone or in combination did not stimulate fetal adrenocortical cell growth, except for a 41% cell number increase by progesterone. Platelet-derived growth factor and insulin-like growth factors I and II were not mitogenic for these cells. These results show that the placenta contains a potent growth factor for human fetal adrenocortical cell cultures. This implies a direct role for the placenta in control of this fetal organ's growth, which would make the human feto-placental unit a bi-directional relationship.

Adrenal Cortex↗
PubMed2002

Growth hormone and prolactin--molecular and functional evolution.

Growth hormone, prolactin, the fish hormone, somatolactin, and related mammalian placental hormones, including placental lactogen, form a family of polypeptide hormones that share a common tertiary structure. They produce their biological effects by interacting with and dimerizing specific single transmembrane-domain receptors. The receptors belong to a superfamily of cytokine receptors with no intrinsic tyrosine kinase, which use the Jak-Stat cascade as a major signalling pathway. Hormones and receptors are thought to have arisen as a result of gene duplication and subsequent divergence early in vertebrate evolution. Mammalian growth hormone and prolactin show a slow basal evolutionary rate of change, but with episodes of accelerated evolution. These occurred for growth hormone during the evolution of the primates and artiodactyls and for prolactin in lineages leading to rodents, elephants, ruminants, and man. Placental lactogen has probably evolved independently on three occasions, from prolactin in rodents and ruminants and from growth hormone in man. Receptor sequences also show variable rates of evolution, corresponding partly, but not completely, with changes in the ligand. A principal biological role of growth hormone, the control of postnatal growth, has remained quite consistent throughout vertebrate evolution and is largely mediated by insulin-like growth factors. Prolactin has many and diverse roles. In relation to lactation, the relative roles of growth hormone and prolactin vary between species. Correlation between the molecular and functional evolution of these hormones is very incomplete, and it is likely that many important functional adaptations involved changes in regulatory elements, for example, altering tissue of origin or posttranscriptional processing, rather than change of the structures of the proteins themselves.

Animals↗
PubMed1989

Aromatase cytochrome P450 and cholesterol side-chain cleavage cytochrome P450 in corpora lutea of pregnant rats: diverse regulation by peptide and steroid hormones.

In previous studies we have shown that aromatase cytochrome P450 (P450arom) mRNA and protein increase markedly in luteal tissue between days 10-19 of gestation, whereas cholesterol side-chain cleavage cytochrome P450 (P450scc) appears to be constitutively maintained regardless of hormonal changes occurring during pregnancy. To identify pituitary and placental hormones that regulate these two P450 enzymes in the rat corpus luteum, serum LH activity and pituitary PRL release were selectively inhibited by administration of LH antiserum (LH-Ab) or CB-154, respectively. Placental hormones were removed by hysterectomy. Hormonal activities were replaced by the administration of hCG, PRL, testosterone (T), or estradiol (E), given individually or in combination. Induction of aromatase mRNA transcripts (3.3, 2.6, and 1.9 kilobases) and protein (54,000 mol wt) between days 10-15 of gestation was blocked by either surgical hysterectomy or LH-Ab treatment. Hysterectomy on day 10 combined with CB-154 abolished not only aromatase mRNA, but also markedly reduced P450scc mRNA (2.0 kilobases) by day 12. Induction of aromatase was partially restored in the day 10-15 hysterectomized rats by treatment with PRL plus E (most effective), PRL plus T, or PRL alone, but not by either T or E alone. Similar results were observed 2 days after hysterectomy (day 12), except that hysterectomy alone caused a transient 3.5-fold increase in P450arom mRNA and protein, most likely due to a transient release of pituitary LH. Aromatase mRNA and protein were also increased in intact pregnant rats treated with hCG between days 10-12. However, no effect of hCG was observed before (days 8-10) or after (days 13-19) midgestation. Likewise, LH-Ab had no effect if given after day 13. Despite hormone-specific regulation of the content of aromatase protein, E biosynthesis in vitro was not strictly related to aromatase enzyme content. We conclude that aromatase mRNA and protein are maintained by PRL at a low level of expression in the first half of pregnancy, can be modulated by LH at midgestation, and are subsequently induced to high levels in the second half of gestation by placental factors (rat placental lactogen-1 and T) and the conversion of T to E in the corpus luteum. P450scc appears to be constitutively maintained. Thus, two P450 genes known to be regulated by LH/cAMP in the rat follicle are controlled by diverse peptide and steroid signal transduction mechanisms in the corpus luteum.

Animals↗
PubMed1983

Two structurally different genes produce the same secreted human placental lactogen hormone.

Experiments were designed to determine if the members of the human placental lactogen (hPL) cluster, consisting of four nonallelic genes, are transcribed in term placenta. Taking advantage of differences in restriction endonuclease sites in the coding portions of the different hPL genes and thus of their putative cDNAs, we have identified two transcriptionally active nonallelic hPL genes in term placenta. The two expressed genes, which code for secreted hPL with identical amino acid sequences, are about equally represented in the hPL mRNA population.

Base Sequence↗
PubMed1990

Placental growth hormone as a potential regulator of maternal IGF-I during human pregnancy.

Ninety-three healthy women were investigated during normal pregnancy, and 177 blood samples were obtained at various gestational stages. In 8 of the women, serial measurements were obtained over a period of 16-34 wk from 8 to 40 wk of gestation. In 13 women, daily blood samples were obtained from day 0 to day 6 after delivery. Insulin-like growth factor I (IGF-I) and human placental lactogen (hPL) were measured by radioimmunoassays. Growth hormone (GH) was estimated by two monoclonal antibody-based radioimmunoassays insensitive to physiological concentrations of hPL: the K24 assay, which recognizes only pituitary hGH, and the 5B4 assay, which reacts with all the known pituitary as well as placental GH variants. Placental GH was distinguished from the main pituitary variant through its specific immunoreactivity pattern. Mean plasma levels of IGF-I were relatively stable until 29-30 wk gestation, then increased progressively to reach a maximum at 35-36 wk. Regardless of gestational age, individual IGF-I values exhibited a highly significant positive correlation with placental GH, reflected by 5B4 immunoreactivity, whereas the correlation between IGF-I and hPL was not statistically significant. Considering each 2-wk gestational period separately, we found a positive correlation between IGF-I and 5B4 hGH at 31-32 wk. Conversely, no evidence of correlation was found between IGF-I and hPL at any period. After delivery, IGF-I evolution exhibited a biphasic pattern, with an initial decrease to low values followed by a progressive return toward levels found in nonpregnant healthy women. These results strengthen our previous hypothesis that placental growth hormone is involved in the control mechanism of serum IGF-I levels in normal pregnant women.

Antibodies, Monoclonal↗
PubMedDate not supplied

Glutathione-S-transferase and NADPH cytochrome P450 reductase activities in rat placenta during pregnancy.

Mammalian gestation depends on the continuous synthesis of steroid hormones such as progesterone, estrogens and gonadotrophic hormones. Placental microsomes are involved in the metabolism of steroid hormones via NADPH cytochrome P450 reductase; this last enzyme is involved in the generation of O2 and H2O2. These partially reduced oxygen forms are scavenged by endogenous antioxidants such as GSH and the related GSH-S-transferase enzyme. The present study has the aim of evaluating whether placental hormonal modification occurring during gestation influences NADPH cytochrome P450 reductase and GSH-S-transferase activities. The results demonstrate a gradual increase of both enzymatic activities which suggests a defense ability of the placenta.

Animals↗
PubMed1996

A monoclonal antibody to human placental lactogen hormone facilitates isolation of fetal cells from maternal blood in a model system.

A cocktail of trophoblast-reactive monoclonal antibodies (MAbs) is required for efficient isolation of trophoblasts from maternal blood. A modified antibody screening procedure was used to identify a clone, in a COS cell placental cDNA expression library, that expressed the gene product recognized by MAb FDO202N. The antigen recognised by MAb FDO202N was identified as human placental lactogen (hPL) hormone. hPL hormone is secreted into the maternal blood by trophoblasts at high levels during pregnancy. Immunohistochemical localization of hPL hormone was consistent with expression in the syncytiotrophoblast and extravillous cytotrophoblast. A model system was used where known numbers of syncytiotrophoblast sprouts were seeded into saline or maternal blood, bound by trophoblast-specific MAbs, recovered magnetically, and then counted. MAb FDO202N was shown to facilitate the efficient recovery of trophoblast sprouts from saline and maternal blood.

Animals↗
PubMed1995

Effect of insulin on endocrine pancreas function during late pregnancy in the rat.

To partly or completely satisfy the increasing demand for insulin, pregnant rats were infused SC with human insulin (2.4 or 4.8 IU/day) from day 14 to day 20 of gestation. Cyclic control rats underwent the same procedure of 6 days of insulin-treatment. During the treatment all groups of rats were hypoglycaemic, but foetal survival was not affected. The low dose treatment prevented the characteristic rise of the insulin response to a glucose challenge during pregnancy, both in vivo and in vitro, while the high dose treatment suppressed the insulin response, as well as the pancreatic insulin content. The insulin responses and insulin contents of pregnant rats were higher than those of the corresponding cyclic control rats. These results support the hypothesis that during gestation the increased insulin demand, due to the actions of placental hormones, is the cause of the increased insulin secretion. However, it cannot be excluded that direct effects of placental hormones on the islets of Langerhans are also involved.

Animals↗
PubMed1995

Retinoic acid and thyroid hormone regulate placental lactogen expression in human trophoblast cells.

In this study, we have demonstrated that retinoic acid (RA) and thyroid hormone (T3) stimulate the synthesis and release of human placental lactogen (hPL), one of the major secretory products of syncytiotrophoblast cells. Enzymatically, dispersed trophoblast cells from term placentas exposed continuously to RA (0.5 microM) and T3 (0.1 microM) for 5 days released significantly more hPL than control cells after 3 days of exposure (P < 0.001 in each instance). On days 4 and 5, the amounts of hPL released by cells exposed to RA and T3 were approximately 3- and 5-fold higher than those in control cells, respectively. The stimulation by both RA and T3 was dose dependent and was accompanied by stimulation of hPL messenger RNA levels. RA and T3 caused 3.5- and 5.6-fold increases, respectively, in chloramphenicol acetyltransferase activity in BeWo choriocarcinoma cells transfected transiently with a 2.3-kilobase (kb) fragment of the hPL promoter (-2300 to 2 basepairs) coupled to a chloramphenicol acetyltransferase reporter gene. Deletion construct analysis of the hPL promoter (2.3, 1.2, and 0.5 kb) indicated that the T3- and RA-responsive elements are localized -0.5 to -1.2 kb up-stream from the transcriptional start site (+1), where several consensus RA- and T3-responsive element sites are present. These results indicate that RA and T3 stimulate the synthesis and release of hPL by a mechanism involving hPL gene transcription and further support a role for these steroids in placental function.

Base Sequence↗
PubMed1987

The lipolytic effects of mouse placental lactogen II, mouse prolactin, and mouse growth hormone on adipose tissue from virgin and pregnant mice.

The lipolytic activities of three structurally related mouse hormones, placental lactogen II (mPL-II), GH (mGH), and PRL (mPRL), and human PL (hPL) were investigated. Adipose tissue was obtained from virgin and day 12 and day 16 pregnant mice. Lipolytic activity was assessed by the ability of the hormones to stimulate glycerol release from fat explants in the presence of dexamethasone and by the ability of the hormones to sensitize adipose tissue to the lipolytic stimulus theophylline. In the first experiment, adipose tissue explants were incubated in Krebs-Ringer buffer with 0.0, 0.1, 0.5, 1.0, 5.0, and 10.0 micrograms/ml hormone for 4 h. mGH was lipolytic at a concentration of 0.5 micrograms/ml or greater in adipose tissue from both virgin and pregnant mice. mPRL was lipolytic at a concentration of 5.0 micrograms/ml or greater in adipose tissue from virgin mice. In adipose tissue from pregnant mice mPRL was not lipolytic in day 12 tissue, but it was lipolytic at a concentration of 5.0 micrograms/ml in day 16 tissue. mPL-II and hPL did not stimulate glycerol release in mouse adipose tissue from virgin or pregnant mice. In the second experiment preincubating adipose tissue from virgin mice in the presence of 0.5 or 5.0 micrograms/ml mGH significantly increased the ability of the tissue to respond to theophylline; however, mGH did not induce this response in adipose tissue from pregnant mice, mPRL, mPL-II, and hPL did not increase theophylline-induced lipolysis in adipose tissue from either virgin or pregnant mice. These results indicate that two lipolytic mechanisms are activated in adipose tissue from mice; mGH can activate both mechanisms, whereas mPRL can activate only one.

Adipose Tissue↗
PubMed2002

TNF-alpha is a predictor of insulin resistance in human pregnancy.

Historically, insulin resistance during pregnancy has been ascribed to increased production of placental hormones and cortisol. The purpose of this study was to test this hypothesis by correlating the longitudinal changes in insulin sensitivity during pregnancy with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha. Insulin resistance was assessed in 15 women (5 with gestational diabetes mellitus [GDM] and 10 with normal glucose tolerance) using the euglycemic-hyperinsulinemic clamp procedure, before pregnancy (pregravid) and during early (12-14 weeks) and late (34-36 weeks) gestation. Body composition, plasma TNF-alpha, leptin, cortisol, and reproductive hormones (human chorionic gonadotropin, estradiol, progesterone, human placental lactogen, and prolactin) were measured in conjunction with the clamps. Placental TNF-alpha was measured in vitro using dually perfused human placental cotyledon from five additional subjects. Compared with pregravid, insulin resistance was evident during late pregnancy in all women (12.4 +/- 1.2 vs. 8.1 +/- 0.8 10(-2) mg. kg(-1) fat-free mass. min(-1). microU(-1). ml(-1)). TNF-alpha, leptin, cortisol, all reproductive hormones, and fat mass were increased in late pregnancy (P < 0.001). In vitro, most of the placental TNF-alpha (94%) was released into the maternal circulation; 6% was released to the fetal side. During late pregnancy, TNF-alpha was inversely correlated with insulin sensitivity (r = -0.69, P < 0.006). Furthermore, among all of the hormonal changes measured in this study, the change in TNF-alpha from pregravid to late pregnancy was the only significant predictor of the change in insulin sensitivity (r = -0.60, P < 0.02). The placental reproductive hormones and cortisol did not correlate with insulin sensitivity in late pregnancy. Multivariate stepwise regression analysis revealed that TNF-alpha was the most significant independent predictor of insulin sensitivity (r = -0.67, P < 0.0001), even after adjustment for fat mass by covariance (r = 0.46, P < 0.01). These observations challenge the view that the classical reproductive hormones are the primary mediators of change in insulin sensitivity during gestation and provide the basis for including TNF-alpha in a new paradigm to explain insulin resistance in pregnancy.

Adult↗
PubMed1990

The human placental growth hormone variant is mitogenic for rat lymphoma Nb2 cells.

Although there is evidence that human (h) placental GH variant (hGH-V) possesses a growth-promoting function, lactogenic activity by the hormone has not been demonstrated. Rat anterior pituitary tumor (GC) cells stably transfected with the hGH-V gene (GC [hGH-V] cells) synthesize and secrete hGH-V. This hormone shares considerable structural similarity with pituitary growth hormone (hGH-N) and chorionic somatomammotropin (hCS) at the nucleotide (greater than 90%) and amino acid (greater than 80%) levels. As expected, both hGH-N and hCS antibodies detect hGH-V by immunoblotting. However, hGH-V, but not hGH-N or hCS, cross-reacts with human or rat pituitary prolactin (PRL) antibodies. These data indicate that structural features shared by hGH-V and pituitary PRL are not present in hGH-N or hCS. Comparison of amino acid sequences implicates two regions that may account for a common epitope between hGH-V and hPRL, and structural difference from hGH-N and hCS. The possible lactogenic activity by hGH-V was assessed in a rat lymphoma Nb2 cell bioassay. Conditioned medium from GC[hGH-V] cells permitted growth of lactogen-dependent Nb2 lymphoma cells in culture. This activity was blocked by antibodies raised to rat PRL but not hPRL or hGH-N. Comparison of the hGH-V amino acid sequence with those from 14 other lactogenic hormones, including hPRL, hCS and hGH-N, reveals 6 conserved amino acids. These data indicate a lactogenic as well as growth-promoting function for the secreted hGH-V protein in vivo.

Amino Acid Sequence↗
PubMed1989

[Endocrine function of the feto-placental complex in anemia of varying degrees of severity].

To assess the endocrine performance of the fetoplacental system in anemia-complicated pregnancy, blood levels of dehydroepiandrosterone sulfate (DEAS), estriol (E3), estradiol (E2), progesterone (PRG) and placental hormone were studied in 287 normal women and female patients with varying anemias. Increased levels of PRG found in the blood of anemic patients were suggestive of a higher endocrine performance of their placentas. In this line, anemic females demonstrated relatively high blood concentrations of E3 and E2 despite dramatical drop in DEAS levels. In patients with severe anemia two late months of gestation were featured by lowered hormonal preformance in the placenta as well as lower levels of PRG, placental hormone, E3 and E2.

Anemia↗
PubMed1990

Placental steroid hormones.

The intent of this review was a selective consideration of recent advances in understanding placental steroidogenesis in humans. While we have omitted material, both intentionally and unintentionally, we hope this discourse presents a flavour of the current molecular endocrinology of placental steroidogenesis. In particular, advances in knowledge as it relates to the enzymes involved in progesterone and oestrogen metabolism have been addressed and correlated with placental development. Finally, because relatively less is known about regulation of steroidogenesis in the human placenta beyond the aspects of growth and differentiation, we have discussed regulation in general terms using recent data obtained in animal species.

Androstenedione↗
PubMed2004

Colloidal effect of albumin on the placental lactogen and chorionic gonadotrophin releases from human term placental explants.

Albumin has been reported to stimulate the release of placental lactogen and chorionic gonadotrophin from human term placental explants within physiological concentrations. This study aimed at characterizing further its effect on the placental hormonal secretion. The placental lactogen and chorionic gonadotrophin secretory response of incubated explants to 5% albumin was reproduced by colloidal agents, i.e., dextran (4.5%) and polygelin (4%), indicating that a rise in colloidal osmotic pressure can elicit hormonal release from the syncytiotrophoblast. Their secretory effects were not modified by the absence of extracellular calcium or the presence of verapamil in the medium. The three agents also provoked a marked increase in (45)calcium outflow from preloaded and perifused explants that persisted in absence of extracellular calcium. These data indicate that the triggering effect of albumin on placental lactogen and chorionic gonadotrophin release can be partly reproduced by colloidal agents and is independent of extracellular calcium.

Albumins↗