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PubMedDate not supplied

Gestational age-related inhibition of placental hCG, alpha hCG and steroid hormone release in vitro by a GnRH antagonist.

Human placental tissues have been shown to contain gonadotrophin-releasing hormone-(GnRH)-like activity. Thus, the effect of a potent GnRH antagonist (N-Ac-Pro1,D-p-Cl-Phe2,D-Nal(2)3,6-GnRH, obtained from Syntex Laboratories) on placental hormonal release was studied. Explant cultures of placentae of 6 to 15 weeks' gestation were studied. This GnRH antagonist did not inhibit the alpha human chorionic gonadotrophin (alpha hCG), human chorionic gonadotrophin (hCG), oestrone or oestradiol release from the six- and nine-week placental cultures, but greatly suppressed the release of these hormones in the placental cultures from 13- and 15-week gestations. Synthetic GnRH partially reversed the action of this antagonist on the hormonal releases in the 15-week placental cultures. These data demonstrate a gestational age-related action of this antagonist on placental hormonal release. Thus, a role for the endogenous GnRH-like activity of the placenta in the control of placental hormonogenesis is indicated.

Chorionic Gonadotropin↗
PubMed1994

Human placental gonadotrophin-releasing hormone (GnRH) binding sites: III. Changes in GnRH binding levels with stage of gestation.

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.

Buserelin↗
PubMed1993

[Simulating and inhibiting effect of individual blood serum transport proteins on thyroid hormone binding with human placental cell membrane].

Binding processes in in vitro systems modelling specific interactions between transport and receptor proteins, thyroid hormones of human placental tissue and the washing blood, have been studied. These systems included syncytiotrophoblast villous membranes, thyroxine (T4), triiodothyronine (T3) and iodothyronine-binding proteins: transthyretin, albumin, immunoglobulins (Ig) M and G, apolipoprotein A-I, and the T4-binding globulin purified from human retroplacental serum. All of the transport proteins at concentrations close to the Ka values of their complexes with thyroid hormones produced inhibitory effects on the binding of [125I]T3 or [125I]T4 to the thyroid hormone membrane receptor. The dependence of [125I]T4 membrane binding on IgM concentration in the system was characteristic of all proteins studied. In the case of T3 such dependence was unique for IgM, and included the phase of the IgM stimulatory effect (10(-11)-10(-9) M) and the phase of inhibition (10(-8)-10(-7) M). In the presence of 30 pM IgM, the concentration of the membrane T3-binding sites increased by 75% with a 2.2-fold decrease of the association constant (Ka). It was shown that IgM interacts specifically with two classes of binding sites on the plasma membranes with Ka(1) = 5.0 x 10(9) M-1, Bmax(1) = 34 fmol/mg of membrane protein and Ka(2) = 2.7 x 10(7) M-1, Bmax(2) = 2.0 pmol/mg of membrane protein. It is suggested that the stimulatory effect of IgM is caused by increases in the number of T3-binding sites on the placental villous membranes as a result of complex formation between IgM and its membrane receptor which displays an enhanced T3-binding activity.

Binding Sites↗
PubMed1971

Where the hormones.

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Amino Acid Sequence↗
PubMed1990

Purified first and third trimester placental trophoblasts differ in in vitro hormone secretion.

In vitro studies with cytotrophoblasts obtained from term placentas have shown low levels of placental protein hormone secretion during the first 2 days in culture, followed by a marked increase during days 3 and 4. Since maternal serum placental hormone levels at term and during the first trimester differ, it is conceivable that cytotrophoblasts from first trimester placentas will differ in endocrine function from those derived from term placentas. Therefore, we examined the secretion of hCG, hCG alpha, human placental lactogen (hPL), and progesterone (P) both in the basal state and after exposure to 8-bromo-cAMP or endogenous cAMP stimulation with cholera toxin in cytotrophoblasts purified by enzymatic dispersion and Percoll gradient centrifugation from four first trimester and four third trimester placentas. At the time of seeding, all cells were mononuclear, and the degrees of aggregation and syncytia formation were similar in first and third trimester trophoblasts during the 4 days in culture. First trimester trophoblasts secreted greater quantities of hCG than did term trophoblasts, while basal secretion of hCG alpha, hPL, and progesterone were similar. Qualitative differences in the hormone secretory patterns were apparent. hCG secretion by first trimester trophoblasts decreased over the 4 days in culture, while the amounts secreted by third trimester trophoblasts increased. hCG alpha levels increased for 2-3 days in first trimester trophoblasts and then decreased, while hCG alpha increased in term trophoblast medium over the 4 days. The ratio of hCG alpha to hCG in media from first and third trimester cultures reflected the relative ratios of these hormones in placental tissue and maternal serum at analogous stages of pregnancy. hPL concentrations in the medium declined between days 3-4 in first trimester cultures, while they increased between days 3-4 in third trimester cultures. The secretory pattern of P was somewhat more erratic. cAMP stimulation led to a similar rise in hCG, hCG alpha, and P secretion in first and third trimester trophoblasts, and a variable response for hPL secretion. These results indicate that the functional activity of placental trophoblasts in culture depends in part upon the age of the placenta from which the cells are derived. The differences may represent intrinsic differences in function or the presence of inhibitory or stimulatory factors of maternal, fetal, or trophoblast origin.

Adult↗
PubMedDate not supplied

Placental villous glucose metabolism and hormone release respond to varying oxygen tensions.

OBJECTIVE: The effects of varying oxygen tensions on tissue metabolic behavior are not well understood, yet many intracellular pathways are influenced by them. In the placenta, optimal in vivo oxygen tension at the villous level is unknown. The purpose of this study was to determine effects of varying oxygen tensions on glucose metabolism and hormone release from perifused placental villous explants. METHODS: Placentas from term normal pregnancies (n = 8) were individually minced into villous fragments, placed into three parallel chambers for each placenta, and continuously perifused for 6 hours with nonrecirculating medium aerated with either 0%, 20%, or 95% oxygen yielding mean oxygen tensions of 76 mmHg, 167 mmHg, and 543 mmHg respectively. Outflow medium was removed at regular intervals and compared to the inflow medium to determine oxygen and glucose consumption as well as lactate, lactate dehydrogenase, hCG, estradiol, and progesterone release. RESULTS: Oxygen consumption was directly proportional to oxygen tension. Glucose consumption was lowest at low oxygen tension, while both lactate and LDH release were lowest at high oxygen tension. Both hCG and progesterone release rates were lowest at high oxygen tensions. Estradiol release demonstrated a trend similar to that of the other hormones although there was no statistically significant difference among the three different levels of oxygen tension. CONCLUSION: Varying oxygen tensions affect placental villous glucose metabolism and hormone release. Under lower oxygen tensions, glucose is metabolized through glycolysis rather than through oxidative phosphorylation and is associated with higher lactate release. Exposure to higher oxygen tensions results in reduced hCG and progesterone release. Higher oxygen tensions may be associated with tissue toxicity.

Chorionic Gonadotropin↗
PubMed1970

Factors affecting the response to insulin in the normal subhuman pregnant primate.

The concentrations of plasma glucose, free fatty acids, insulin, growth hormone, and placental prolactin in subhuman primate fetal and maternal plasma were examined following intravascular administration of insulin and glucagon to the fetus and mother. The neonatal plasma responses to these same stimuli were also examined. Fetal plasma glucose concentrations were minimally altered by direct fetal insulin injections, whereas neonatal glucose levels declined with similar injections. In both instances, however, plasma free fatty acid levels declined following insulin. When the amount of insulin given the fetus was increased, fetal plasma glucose concentrations did decline. Combined intravascular insulin injections and infusions in the mother were associated with a disappearance of the initial maternal to fetal plasma glucose concentration gradient and a nearly parallel fall in both maternal and fetal plasma glucose levels. It was concluded that insulin was biologically active in the fetus. Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Maternal plasma placental prolactin and fetal plasma growth hormone levels were unchanged in the presence of sustained maternal and fetal hypoglycemia. However, neonatal plasma growht hormone levels did increase in response to hypoglycemia. The observed bidirectional placental barrier to transfer of radioisotopically labeled growth hormone indicated that fetal plasma growth hormone was solely of fetal origin. These data suggested further that a change in the growth hormone-releasing mechanism may occur from fetal to neonatal life. Direct maternal intravascular glucagon administration led to augmentation in both maternal and fetal plasma insulin and glucose levels. Direct fetal glucagon injections enhanced both maternal and fetal plasma insulin levels. These simultaneous changes in both plasma pools were consistent with the demonstration of a bidirectional placental transfer of radioisotopically labeled glucagon. The role of endogenously produced glucagon in these studies remains to be clarified.

Animals↗
PubMed2000

Placental lactogen not growth hormone and prolactin regulates secretion of progesterone in vitro by the 40-45 day ovine corpus luteum of pregnancy.

The study was designed to compare the direct effect of three prolactin-like hormones on steroidogenesis of ovine luteal cells collected at day 40-45 of pregnancy. 100 ng/ml of ovine placental lactogen or 100 ng/ml of ovine growth hormone or 100 ng/ml of ovine prolactin were added to the media of luteal cell cultures. After 48 h incubation, all cultures were terminated and the media were frozen until further steroid analysis. To determine to what extent growth hormone (GH), prolactin (PRL) and lactogen (PL) regulate the activity of 3 beta-HSD, an enzyme involved in progesterone synthesis, the classical steroidal competitive inhibitor of 3 beta-HSD trilostane, was investigated for its effects on basal and GH-, PRL-, and PL-stimulated progesterone biosynthesis since there is a possibility that the luteotropic effect of these hormones are mediated via 3 beta-HSD. oPL resulted in an increase of progesterone secretion in a statistically significant manner, while GH or PRL had no effect on progesterone secretion. A decrease in progesterone secretion as an effect of 100 mM trilostane was observed in all culture types. An explanation for the luteotropic effect of PL and the lack of this effect for GH is that the GH receptor associates with a different molecule within the ovarian tissue and forms a heterodimeric receptor for PL, and the possibility that physiological effects of native oPL may be mediated through its binding to specific PL receptors, which have low affinities for oGH and oPRL.

3-Hydroxysteroid Dehydrogenases↗
PubMed1987

Effects of continuous intravenous infusion of an ovine placental extract enriched in placental lactogen on plasma hormones, metabolites and metabolite biokinetics in non-pregnant sheep.

Continuous intravenous infusions of saline or of a placental extract containing ovine placental lactogen were given to three non-pregnant, non-lactating ewes over periods of 36 h, 1 week apart. During saline infusion no placental lactogen was detected in jugular vein plasma. but infusion of the placental extract raised the placental lactogen concentration from undetectable to 40-50 micrograms/l, similar to concentrations in ewes with one fetus on day 90 of pregnancy. By comparison with the saline control period, infusion of the placental extract consistently increased both plasma concentrations and irreversible loss of nonesterified fatty acids. Plasma concentrations of glucose and urea, but not irreversible loss of these metabolites, were consistently increased. Although the placental extract was not subjected to extensive purification, it was enriched in placental lactogen and contained no detectable contamination with insulin, prolactin or growth hormone. The results are suggestive of a role for placental lactogen in modifying metabolism and acting during pregnancy to provide nutrients for fetal metabolism.

Animals↗
PubMed1995

Cocaine-sensitive sigma-receptor and its interaction with steroid hormones in the human placental syncytiotrophoblast and in choriocarcinoma cells.

The expression and ligand binding characteristics of sigma-receptors in human placental syncytiotrophoblast and choriocarcinoma cells were investigated using haloperidol as a ligand. Haloperidol bound to purified placental brush border membranes with high affinity; the apparent dissociation constant for the process was about 3 nM. These binding sites were not related to dopamine (D2) and serotonin (5-HT2) receptors nor to serotonin and norepinephrine transporters. The ligands of sigma-receptors [3.g. (+)-3-(3-hydroxyphenyl)N-(1-propyl)piperidine, 1,3-di-(2-tolyl)guanidine, clorgyline, rimcazole, and dexromethorphan] were very potent in competing with haloperidol for the binding sites. The binding sites were detected not only in the brush border membrane, but also in intracellular membranes. The rank order of potency of various sigma-receptor ligands to inhibit haloperidol binding indicated that placental sigma-receptors belong to the sigma 1 subtype. Cocaine and its analog RTI-55 [2 beta-carbomethoxy-3 beta-(4-iodophenyl-) tropane] inhibited the binding of haloperidol to placental membranes with appreciable potency. The steroid hormones, progesterone and testosterone, were also potent inhibitors, and the inhibition constant for progesterone was 0.3 microM, a concentration much smaller than that found in plasma during pregnancy. The inhibition was competitive. beta-Estradiol and a number of other steroids were relatively much weaker inhibitors than progesterone and testosterone. Phenytoin and neuropeptide-Y did not interact with sigma-receptors in placenta. The choriocarcinoma cell line JAR was also found to express sigma-receptors in the plasma membrane as well as in intracellular membranes. The characteristics of the receptors in this cell were qualitatively similar to those of the receptors in normal placenta, including subtype identity and interaction with cocaine and progesterone. Interestingly, however, all sigma-receptor ligands interacted with the receptors in the JAR cell with much higher affinity than with the receptors in normal placenta. It is concluded that the placental syncytiotrophoblast and choriocarcinoma cells express cocaine-sensitive sigma-receptors and that progesterone is most likely an endogenous ligand for these receptors.

Choriocarcinoma↗
PubMed1995

Tumor necrosis factor-alpha affects in vitro hormone production by JEG-3 choriocarcinoma cell cultures.

Steroid hormones, produced by the placenta, appear to be critically important in maintaining the pregnancy of experimental animals and possibly humans. Previous studies in our laboratory have shown that macrophage-conditioned media, which are known to contain several cytokines including tumor necrosis factor-alpha (TNF-alpha), decreased the in vitro synthesis of progesterone (P) and increased the synthesis of estradiol (E2) by placental fragments. The present study was designed to further our understanding of the effect of cytokines on the synthesis of placental trophoblast hormones. The current study shows that TNF-alpha (1-20 ng/ml) decreases the in vitro synthesis of P and increases the synthesis of both E2 and human chorionic gonadotropin (hCG) by JEG-3 choriocarcinoma cells (a model for trophoblast hormone synthesis). The effects of TNF-alpha are independent of changes in formation of adenosine 3':5' cyclic-monophosphate, guanosine 3':5' cyclic-monophosphate, prostaglandin E2, and prostaglandin F2 alpha. However, the effect of TNF-alpha on P formation is blocked by cycloheximide (1 microgram/ml). These observations suggest TNF-alpha could have effects on placental hormone synthesis which might be important in the pathogenesis of both normal and preterm labor. At least some of these effects appear mediated through new protein synthesis.

Choriocarcinoma↗