[Studies on the effects of adrenal cortex hormones on placental functions, especially nucleic acid synthesizing capacity].
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Animals↗
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[Maternal glucose tolerance along pregnancy (author's transl)].
The development of the foetal and placental unit induces large changes in maternal glucose tolerance along pregnancy. Oestrogen-induced hyperinsulinism is responsible for facilitated anabolism which take place during the first part of pregnancy. Accelerated catabolism occurring during the second part is due to the direct action of placental hormones, mainly of human placental lactogen. The latter is responsible for diminution of peripheral insulin activity. Hyperinsulinism, which is very important at this stage, facilitates an intense and rapid anabolism, mainly in the liver from where nutriments can be easily removed. Glucose and amino-acid uptake by placental and foetus are greatly increased by all these changes.
Blood Glucose↗
[Assessment of the detection of pregnancy-specific hormones (human placental lactogen and beta-1-glycoprotein) in breast exudates in mastopathy and breast cancer].
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Adenocarcinoma↗
[Maternal glucose tolerance along pregnancy (author's transl)].
The development of the foetal and placental unit induces large changes in maternal glucose tolerance along pregnancy. Oestrogen-induced hyperinsulinism is responsible for facilitated anabolism which take place during the first part of pregnancy. Accelerated catabolism occurring during the second part is due to the direct action of placental hormones, mainly of human placental lactogen. The latter is responsible for diminution of peripheral insulin activity. Hyperinsulinism, which is very important at this stage, facilitates from where nutrients can be easily removed. Glucose and amino-acide uptake by placental and foetus are greatly increased by all these changes.
Amino Acids↗
Corticotrophin releasing hormone: its potential for a role in human myometrium.
Aside from its role as a hypothalamic stress hormone, corticotrophin releasing hormone (CRH) is also a placental hormone, at least in primates. Although the function of placentally derived CRH remains to be fully elucidated, elevated CRH levels have been associated with premature labour, suggesting that the hormone may be involved in regulating the duration of pregnancy. Indeed, pregnant human myometrium expresses functional CRH receptors (CRH R1 and CRH R2 subtypes) thought to signal predominantly via the second messenger cAMP. Thus, like other cAMP-producing hormones in the myometrium such as beta(2) agonists, CRH may play a part in maintaining uterine quiescence. However, several of the CRH receptor isoforms identified to date have a reduced ability to activate adenylate cyclase, raising the question as to whether they are linked to other signal transduction pathways. Here, we discuss critically the evidence for the peptide's role in regulating contractility, both directly at the myometrium and indirectly via the fetal membranes and decidua. The possibility of a role in myometrial growth modulation is also described. Experimental Physiology (2001) 86.2, 273-281.
Corticotropin-Releasing Hormone↗
Chorionic gonadotrophin and c-myc expression in growing and growth-inhibited (intermediate) trophoblasts.
FEG-3 cells are a clonal line of human choriocarcinoma and resemble villous cytotrophoblasts which are the stem cells for the syncytiotrophoblast in the placenta. FEG-3 cells synthesize and secrete the alpha subunit of human chorionic gonadotrophin (hCG). Treatment of FEG-3 cells with the chemotherapeutic drug (1 microM) methotrexate (MTX) results in an increase in nuclear diameter. Cell division is blocked and a decrease in c-myc mRNA levels in observed. The effects on cell growth and c-myc mRNA expression are reversible, and cells treated with MTX for 48 h retain their proliferative potential. Assessment of placental hormone gene expression reveals that a member of the human growth hormone gene family is expressed at extremely low levels and is unaffected by MTX treatment. Alpha and beta chorionic gonadotrophin (hCG) levels are increased by MTX treatment, but levels decrease following removal of MTX. In contrast to hCG in FEG-3 cells, non-trophoblastic or ectopic production of alpha hCG in human cervical carcinoma cells is inhibited by MTX treatment. These data indicate that MTX will induce morphological and biochemical changes in FEG-3 cells. They reveal an inverse relationship between c-myc and hCG RNA expression, and suggest different mechanisms govern trophoblast versus non-trophoblast production of alpha hCG.
Actins↗
Leptin in human pregnancy: the relationship with gestational hormones.
OBJECTIVES: The aims of the study were (1) to examine the relationship between leptin and placental hormones by measuring serial changes in serum levels of leptin during and after pregnancy and (2) to study the effects of several gestational hormones on leptin release from fully differentiated 3T3-L1 adipocyte cell cultures. STUDY DESIGN: Serum levels of leptin were measured throughout pregnancy and at 3 months post partum in 29 healthy women and were also measured in 18 healthy women at delivery by cesarean section and on postpartum day 3. In addition, 3T3-L1 mouse adipocytes were incubated for 24 hours in media containing various reproductive hormones and leptin production was measured. RESULTS: Serum leptin levels increased significantly (8.4 +/- 0.9 vs 13.5 +/- 1.5 ng/mL; P <.001) between the first 2 trimesters of pregnancy but not between the second and third trimesters. These changes in leptin did not correlate significantly with changes in body mass index. Leptin levels dropped significantly during the immediate postpartum period, from 34.1 +/- 4.9 at cesarean delivery to 7.3 +/- 1.4 ng/mL on postpartum day 3 (P <.001). Fasting insulin level did not correlate significantly with leptin level during pregnancy but did so during the postpartum period (r = 0.60; P <.05). Leptin secretion from 3T3-L1 adipocytes was increased significantly when cells were cultured with human chorionic gonadotropin (150%, P <.01) and also when they were cultured with estrogen (120%, P <.03). CONCLUSION: The data suggest that leptin production by adipose tissue is stimulated by several hormones of pregnancy, which may contribute to the increased leptin levels observed during gestation.
3T3 Cells↗
Binding of placental lactogen and growth hormone to fetal sheep fibroblasts.
Growth hormone (GH) regulates growth and development in the postnatal period but lacks somatotropic activity in the fetus. In contrast, the placental hormone placental lactogen (PL) stimulates amino acid transport, DNA synthesis, and somatomedin production in isolated fetal tissues, suggesting that PL may function as a "fetal GH." To elucidate the mechanisms by which PL exerts GH-like effects in fetal tissues, we examined the binding of PL, GH, and prolactin to cultured skin fibroblasts obtained from midgestational fetal lambs. Ovine fetal fibroblasts bound radiolabeled ovine PL (oPL) specifically and with high affinity (EC50 0.20 nM). In competitive displacement assays using 125I-oPL as the radioligand, the potency of unlabeled oPL was eight to 12 times greater than that of ovine GH and congruent to 1000 times greater than that of ovine prolactin. Covalent cross-linking of 125I-oPL (22 kD) to ovine fetal fibroblasts revealed a specific hormone-receptor complex with an apparent M(r) of 130,000, suggesting that the high affinity oPL binding site has a molecular mass of approximately 108 kD. The specific bindings of radiolabeled ovine GH (0.6% per 250 micrograms protein) and ovine prolactin (0.04% per 250 micrograms protein) were only 1/15 and 1/230 that of radiolabeled oPL (9.1% per 250 micrograms protein), and no specific cross-linking of 125I-ovine GH or 125I-ovine prolactin to ovine fetal fibroblasts was detected. These findings demonstrate preferential binding of PL by isolated fetal sheep fibroblasts in culture, providing a cellular mechanism whereby PL may exert growth-promoting effects in the fetus.
Animals↗
Isoimmunization against human chorionic gonadotropin with conjugates of processed beta-subunit of the hormone and tetanus toxoid.
The immunogenicity of the conjugate prepared from "processed" beta-subunit of human chorionic gonadotropin (choriogonadotropin, HCG) and tetanus toxoid has been studied in animals and a human subject. The conjugate elicited the formation of high-affinity (Ka = 10(9)-10(11) M-1) anti-HCG and anti-tetanus antibodies. On primary immunization, the antibody, response lasted for several months. Repeat injection of the conjugate in the declining phase of antibody titers produced a booster response without a lag period. The antibodies reacted with the beta-subunit of HCG and the complete HCG molecule but were devois of significant crossreactivity with human growth hormone, placental lactogen, follicle-stimulating hormone, thyroid-stimulating hormone, and luteinizing hormone at tonic and surge levels. The antibodies were competent for neutralizing the biological activity of HCG in the mouse uterine weight gain assay, the ventral prostate weight gain assay, and the radioligand assay for binding of 125I-labeled HCG to receptors on corpus luteum. HCG (5000 international units) administered to an immunized subject was completely bound by circulating antibodies. Administration of HCG (in contrast to conjugate) was without booster effect on anti-HCG titers.
Animals↗
GATA-2 restricts prolactin-like protein A expression to secondary trophoblast giant cells in the mouse.
An analysis of the pattern of expression of the mouse placental hormone prolactin-like protein A (PLP-A) has revealed that this hormone is expressed exclusively in secondary trophoblast giant cells but not in primary giant cells. Thus, PLP-A serves as a marker for a subset of giant cells. Recent results have indicated that PLP-A binds to and inhibits the activity of natural killer cells, and thus, the localized expression of PLP-A may be important for regulating the activity of this class of T lymphocytes in a restricted region of the implantation site. Previous studies indicated that the transcription factor GATA-2 is required for the trophoblast giant cell-specific expression of two other hormones in the prolactin family, placental lactogen I and proliferin. In the absence of GATA-2, PLP-A continues to be expressed, but in this mutant background, PLP-A mRNA is detected in both primary and secondary giant cells. Thus, GATA-2 contributes both to positive and negative regulation of trophoblast giant cell-specific gene expression, and this factor apparently plays an important role in generating or maintaining the distinct functions of secondary, compared with primary, trophoblast giant cells.
Animals↗
Production of recombinant human placental variant growth hormone in Pichia pastoris.
cDNA encoding mature human placental variant growth hormone (HGH-V) was synthesized by retro-transcription polymerase chain reaction (RT-PCR) from total RNA recovered from human term-placenta and cloned in pBluescript plasmid (pBS) in Escherichia coli. cDNA was subcloned into pPIC9, fusing it to the flanking regulatory sequences of the Pichia pastoris alcohol oxidase 1 gene (AOX1) and finally introduced into the genome of this yeast by homologous recombination. The resulting new recombinant strain produced and secreted, towards the culture medium, mature HGH-V, whose activity was demonstrated in cell culture by the Nb2 proliferation assay.
Biological Assay↗
Linkage arrangement of human placental lactogen and growth hormone genes.
Human placental lactogen (hPL) and growth hormone (hGH) are two hormones thought to have evolved from a common ancestral gene (along with prolactin), yet they have quite different functions and specificities. The nucleic acid sequences of the respective cDNAs of the two genes share considerable homology, as well as the existence of multiple forms of each gene within the genome. In this study we report on the linkage arrangement of several genes from this group. Two hPL-like genes as well as an hGH gene are shown to be linked within a 38-kilobase pair region of DNA. Linkage between a variant hGH gene and an hPL gene is also shown. The orientation and structural organization of these genes was previously established using 5'- and 3'-specific probes from a placental lactogen cDNA clone and detailed restriction endonuclease mapping. Restriction fragments from the overlapping clones were verified by comparison to digests of high molecular weight genomic DNA. In addition, the location of a specific class of repetitive DNA sequences, the Alu family, was mapped on these clones using the recombinant clone BLUR 8. All members of this multigene family have Alu repeat sequences either immediately flanking their 3' or 5' untranslated regions or within their intervening sequences.
Base Sequence↗
The existence during gestation of an immunological buffer zone at the interface between maternal and foetal tissues.
In mammalian pregnancy the trophoblast normally constitutes an uninterrupted boundary of foetal tissue in immediate contact with maternal tissue, including blood in some species, and is the decisive immunological barrier to rejection of the foetus as an allograft. The ability of the trophoblast to function as a barrier evidently results from its capacity to resist immunological attack by either alloantibody or alloimmune cells and to prevent immunocompetent cells from reaching and damaging the foetus but, as yet, there is no general agreement regarding the means by which it exercises these functions. In view of the dramatic hormonal changes that occur during pregnancy and the undisputed involvement of trophoblast in these endocrine events, the possibility exists of an interaction between the hormones of pregnancy and the immunological phenomena. The present account furnishes evidence that endocrine activity at the maternal surface of the trophoblast, the presumptive site of the immunological frontier between foetus and mother, may be a factor in its local survival at implantation. The placental hormones so far known that are capable of blocking the antigen receptor sites of the mother's lymphocytes and thus preventing the latter from reacting with the foetal antigens are the glycoprotein, human chorionic gonadotrophin (HCG) and the polypeptide hormone, human chorionic somatomammotrophin (HCS) or human placental lactogen (HPL), both of which are specific to the human placenta. The origin of these hormones, their spatial distribution and their probable interaction with placental steroid hormones are discussed. It is argued that the place of highest concentration of these hormones is on the surface of the syncytial microvilli and the adjacent caviolae of the apical plasma membrane, as well as on the surfaces of the persisting cytotrophoblastic cells of the basal plate (cytotrophoblastic shell), the cell islands and the septa-precisely where the immunological challenge of the foetal allograft to the maternal host occurs. An explanation is offered for the continuing production of the voluminous quantities of these hormones during human pregnancy.
Animals↗
Placental genes and breast cancer: can the offspring's or father's genotypes predict mother's risk?
Half of the placental genes to which a woman is exposed during pregnancy come from her mating partner. Placental hormones, especially human chorionic gonadotropin and human placental lactogen, are considered to mediate the protective effects of full-term pregnancy and lactation on breast cancer risk. In this paper, variants in a woman's placental human chorionic gonadotropin or human placental lactogen genes, which are easily measurable through her offspring's genotypes, are associated with her breast cancer risk. If this hypothesis is true it would indicate that genotype of a woman's mating partner can affect her breast cancer risk and that offspring's genotype may be useful in predicting such risk. Because the placenta produces a wide range of hormones and enzymes (in addition to human chorionic gonadotropin and human placental lactogen), results supporting this hypothesis could open new dimensions to genetic research for diseases beyond breast cancer (including gynecologic tumors and reproductive and pregnancy-related disorders).
Breast Neoplasms↗
Changes in placental lactogen, beta 1-chorionic gonadotropin, and unconjugated and total estriol levels in the late course of normal human pregnancy.
The levels of human placental lactogen (hPL), beta-human chorionic gonadotropin (beta-hCG), unconjugated estriol (UE3) and total estriol (TE3) were measured radioimmunologically in women along their course of pregnancy. The serum hPL and beta-hCG levels were relatively constant in uncomplicated pregnancy, while UE3 and TE3 significantly rose towards 41 weeks of gestation. There were positive correlations between hPL and beta-hCG (n = 49, r = 0.737, p less than 0.001), and between UE3 and TE3 (n = 49, r = 0.904, p less than 0.0001). The ratios of placental hormones to estriol showed moderate declines towards 41 weeks of gestation. These data suggest that the fetal adrenal function increased toward the term, while the placental peptide hormones decrease or remain unchanged. Determination of serum unconjugated estriol was found to be convenient and useful for monitoring the fetoplacental function.
Chorionic Gonadotropin↗
The neural and neuro-endocrine component of the human thymus. II. Hormone immunoreactivity.
We evaluated the presence of anterior pituitary hormones; follicle-stimulating hormone (FSH) and its beta-subunit (beta-FSH), luteinizing hormone (LH) and its beta-subunit (beta-LH), beta-subunit of thyroid-stimulating hormone (beta-TSH), adrenocorticotropic hormone (ACTH), growth hormone (GH), and prolactin (PRL); the placental hormone human chorionic gonadotropin (hCG); and somatostatin, in paraffin and frozen sections of the human thymus. Epithelial cells in the medulla were immunoreactive for most of these hormones, in varying density and intensity of labeling. The cells labeled varied from epithelial cells surrounding Hassall's corpuscles toward solitary cells or small epithelial aggregates in the medulla. FSH immunoreactivity did occur predominantly in epithelial cells of the cortex, in apparent contrast to the predominant medullary location of cells immunolabeled for beta-FSH. The epithelial nature of FSH-immunoreactive cells was confirmed by two-color immunohistochemistry with anti-keratin antibody. In addition to FSH, some epithelial cells in subcapsule and cortex were labeled by antibodies to beta-FSH, beta-LH, beta-TSH, ACTH, GH, and PRL. Some macrophage-like cells surrounded by a rosette of lymphocytes were immunoreactive for FSH and GH. Some interdigitating reticulum-like cells were labeled by anti-beta-LH. Immunolabeling of lymphocytes was found for hCG, especially lymphocytes in the medulla. Two-color immunohistochemistry with anti-CD3 revealed a strong CD3 expression on hCG-immunoreactive cells, whereas CD3-negative cells were hCG-negative. T cells immunolabeled for hCG were also found in peripheral lymphoid organs.
Adolescent↗
Regulation of hormone production in the human feto-placental unit.
Hormone production in the human feto-placental unit has been studied extensively yet relatively little is known about the regulatory mechanisms involved. A tissue culture approach has been used to examine the effect of potential controlling factors on steroid production by the human mid-term fetal adrenal and mid-term and term placenta. Adrenal. The pituitary peptides corticotropin (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) had the most significant influence on adrenal steroidogenesis in both the fetal and definitive zones. Their effects were not identical: they enhanced dehydroepiandrosterone sulphate (DHA-S) production in a comparable manner but alpha-MSH had much less of a stimulatory effect on cortisol biosynthesis. Medium from homologous fetal pituitary cultures mimicked the effects of alpha-MSH rather than ACTH. Homologous placental culture medium and progesterone enhanced only cortisol production and only in the fetal zone cells. These results demonstrate that specific fetal pituitary and placental factors influence fetal adrenal activity and suggest a functional zonation of the fetal adrenal. Placenta. DHA, DHA-S and 16-hydroxy-DHA stimulated oestrogen biosynthesis while high concentrations of DHA and DHA-S (but not 16-hydroxy-DHA) inhibited progesterone production. Luteinizing hormone-releasing hormone (LRH) inhibited both oestrogen and progesterone biosynthesis. Placental steroidogenesis can therefore be influenced not only by the fetus, through its increasing adrenal output of oestrogen precursors, but also by factors originating within the placenta itself.
Adrenal Glands↗
Demonstration of functional cytokine-placental interactions: CSF-1 and GM-CSF stimulate human cytotrophoblast differentiation and peptide hormone secretion.
The placental syncytiotrophoblast (ST) is a terminally differentiated epithelial cell monolayer that constitutes the outermost boundary between fetal and maternal tissues and performs a variety of synthetic, secretory, and transport functions essential for the maintenance of pregnancy. Although it is known that the ST arises from the underlying germinal layer of mononuclear cytotrophoblasts (Langhans' cells) by a process of cell fusion, the molecular mechanisms involved in this process are unclear. In order to address this question, we have investigated the effects of macrophage colony-stimulating factor (CSF-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF), lymphohemopoietic cytokines implicated in mammalian placental development, on the in vitro morphological and functional differentiation of human trophoblast. Both CSF-1 and GM-CSF stimulated cytotrophoblast aggregation into large multinucleated structures composed of extensive patches of syncytium interspersed with mononuclear cells. Concomitant with this morphological differentiation was upregulation of the production of the placental hormones placental lactogen and chorionic gonadotrophin. Placental fibroblasts derived from the villous stroma that underlies the trophoblastic epithelium were found to produce both GM-CSF and CSF-1 under the control of the trophoblast-derived cytokines IL-1 and TNF alpha. These observations suggest that a network of interrelated cytokines operates within the basal (fetal) aspects of the villous stroma where they are situated to play a significant role in the morphological and functional development of the human placenta.
Cell Differentiation↗