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PubMed2006

Aspects of placental growth hormone physiology.

Placental growth hormone (PGH) has been known for 20 years. Nevertheless, its physiology is far from understood. In this review, basal aspects of PGH physiology are summarised and put in relation to the highly homologous pituitary growth hormone (GH). During normal pregnancy, PGH progressively replaces GH and reach maximum serum concentrations in the third trimester. A close relationship to insulin-like growth factor (IGF)-I and -II levels is observed. Furthermore, PGH levels are positively associated to fetal growth. The potential importance of growth hormone receptors and binding protein for PGH effects is discussed. Finally, the review outlines current knowledge of PGH in pathological pregnancies.

Female↗
PubMed1998

Circulating thyroid hormone concentrations and placental thyroid hormone receptor expression in normal human pregnancy and pregnancy complicated by intrauterine growth restriction (IUGR).

Thyroid hormones are critical to growth and development of the human fetus. Abnormal placental development, a major cause of intrauterine growth restriction (IUGR), is associated with a high perinatal mortality and morbidity. Thyroid status has been postulated to play a role in the pathogenesis of such morbidity. In the present study, we have investigated fetal thyroid function and placental expression of thyroid hormone receptor (TR) alpha and beta variants during normal human pregnancy and in pregnancy associated with IUGR. Measurement of free thyroid hormones and TSH concentrations revealed significant rises in free T4 and free T3 between the second and third trimesters of normal pregnancy. Serum concentrations of free T4 and free T3 were lower in fetuses affected by IUGR, although serum TSH levels were not significantly different. Immunocytochemistry demonstrated the presence of TR alpha1, alpha2, and beta1 proteins within the nuclei of trophoblast and stromal placental cells. Immunostaining for these TR variants increased with increasing gestation in normal placenta. Comparison of IUGR placental samples with normal samples revealed greater immunostaining for TR alpha1, alpha2, and beta1 variants in IUGR. Examination of pretranslational expression of TR alpha1, alpha2, beta1, and beta2 variants by semiquantitative RT-PCR revealed increasing expression of TR alpha1, alpha2, and beta2 messenger RNAs with increasing gestation in normal pregnancy, which "mirrored" post-translational expression. However, and in contrast, there were no significant differences in expression of TR messenger RNAs in normal and IUGR placenta. The present findings of reduction in serum free thyroid hormones and increased expression of TR alpha and beta proteins in association with IUGR highlight the potential importance of thyroid status in influencing long-term fetal outcome in this condition.

Blotting, Western↗
PubMed1987

Biochemical evidence that human placental lactogen and human chorionic gonadotropin are not stored in cytoplasmic secretion granules.

The intracellular storage sites for the human placental hormones placental lactogen (hPL) and chorionic gonadotropin (hCG) are unknown. To determine whether hPL and hCG are stored in cytoplasmic secretion granules, we have compared the localization of hPL and hCG in placental homogenates following differential and density-gradient centrifugations to those of prolactin (PRL) and luteinizing hormone (LH) in human and rat pituitary homogenates. In the differential centrifugation studies, 93.1 +/- 4.1% (mean +/- SE) of the hPL and 79.4 +/- 6.0% of the hCG were detected in the postmicrosomal supernatant of placental homogenates. In contrast, 95-98% of the hPRL and hLH in the pituitary homogenates were detected in particulate fractions. Following centrifugation on sucrose-density gradients, particulate hPL and hCG were distributed diffusely throughout the gradients, while greater than 90% of the pituitary hormones sedimented as single peaks with densities of 1.22 g/cm3. When human placental and rat pituitary tissues were homogenized together prior to differential and density-gradient centrifugations, similar marked differences were observed between the distribution of the placental and pituitary hormones. These results strongly suggest that the placental hormones hPL and hCG, unlike pituitary PRL and LH, are not stored in large secretory granules. Differences in the intracellular storage sites of the hormones may explain, in part, differences in the regulation of peptide hormone secretion by placental and pituitary tissues.

Animals↗
PubMed1990

Human placental lactogenic hormone as a parameter for placental function in renal transplanted women.

In 13 pregnant women with renal transplants the serum concentration of placental hormones were determined in order to show their ability to predict fetal problems especially placental insufficiency. It is shown that the hPL values were increased because of reduced elimination of hPL, presumably in the renal tubuli. In this study the weight of only one newborn was over the 50th percentile in spite of the fact that all but one had hPL values over the 50th percentile and in even 8 pregnancies the values were over the 95th percentile. In most of the growth-retarded fetus's the ratio between hPL and the weight of the newborns was more complex. It is concluded that in renal transplanted pregnant women, hPL as a parameter for the placental function must be used with reservation and is not able to predict placental insufficiency.

Azathioprine↗
PubMed2002

Human placental growth hormone--a review.

Placental growth hormone (PGH) is the product of the GH-V gene, predominantly expressed in the syncytiotrophoblast layer of the human placenta. PGH differs from pituitary growth hormone by 13 amino acids and possesses one glycosylation site. It has high somatogenic and low lactogenic activities. In the maternal circulation from 12-20 weeks up to term, PGH gradually replaces pituitary growth hormone, which becomes undetectable. PGH is secreted by the placenta in a non-pulsatile manner. This continuous secretion appears to have important implications for physiological adjustment to gestation and especially in the control of maternal IGF1 levels. PGH secretion is regulated in vitro and in vivo by glucose. Lower maternal levels of PGH are observed in pregnancies with fetal growth retardation. PGH is one example of a trophoblast hormone, which allows maternal metabolic adaptation to pregnancy. In addition, our recent data on its expression in invasive extravillous trophoblasts suggest that the physiological role of PGH might also include a direct influence of this hormone on placental development via an autocrine or paracrine mechanism.

Adult↗
PubMed1999

Colocalization of leptin receptor (OB-R) mRNA and placental lactogen-II in rat trophoblast cells: gestational profile of OB-R mRNA expression in placentae.

The present study was designed to clarify the cellular localization and expression of leptin receptor(s) [OB-R(s)] mRNA including its splice variants and their correlation with the cells which secrete placental hormone, placental lactogen-II (PL-II), in rat placentae. By in situ hybridization analysis, hybridization signals for OB-Rb and the common extracellular domain of OB-R were first detectable in some cells of the labyrinth zone of the placentae on day 14 of pregnancy and then a lot of cells dispersed in the entire area of the labyrinth zone expressed OB-Rb during the latter half of pregnancy. However, no expression was observed in the decidua and the junctional zone of the placentae during pregnancy. Double staining study revealed that signals for OB-R expressing trophoblast cells showed PL-II immunoreactivity in the labyrinth zone of the placentae. In Northern blot analysis, two bands (2.8 kb and 5.1 kb) of OB-R mRNA expression were observed in the placentae from day 17 to 21 of pregnancy and the expression of both increased markedly up to day 21 of pregnancy. RT-PCR analysis revealed that OB-Rb, OB-Ra, and OB-Re are expressed in the placentae on days 19 and 21 of pregnancy. These results suggest that the OB-R may have a physiological significance in the placental function during the latter half of pregnancy.

Alternative Splicing↗
PubMed1977

The use of hormones in reproductive management of the mare.

A brief review is presented of the use in equine veterinary medicine of anterior pituitary hormones, posterior pituitary hormones, placental hormones, steroid hormones and prostaglandins. These hormones are used frequently in clinical application without a scientific basis for their expected activity.

Animals↗
PubMed1991

Tissue-specific expression and thyroid hormone regulation of the endogenous placental growth hormone variant and chorionic somatomammotropin genes in a human choriocarcinoma cell line.

Human (h) placenta-derived choriocarcinoma cell lines (BeWo, JAR, and JEG-3) were examined for expression of pituitary GH (hGH-N) as well as placental GH variant (hGH-V) and chorionic somatomammotropin (hCS, encoded by the hCS-A or hCS-B gene). RNA was isolated and assessed using hGH-N complementary DNA since hGH and hCS genes share more than 90% sequences similarity. The relative expression is BeWo greater than JAR greater than JEG-3. In BeWo cells expression of placental hCS-A, hCS-B, and hGH-V genes, but not pituitary hGH-N, is observed using polyadenylated RNA and oligonucleotide probes specific for the different family members. The absence of hGH-N expression in BeWo cells is not due to deletion or gross rearrangement of the gene. No difference was seen between the hGH/hCS genes in genomic DNA from these cells and the DNA from placenta and pituitary when analyzed by restriction digestion and blotting. Treatment of BeWo cells with 10 nM T3 results in a 6-fold increase in messenger RNA from placental members of the hGH gene family. Levels of hCS-A, hCS-B, and hGH-V transcripts are all elevated. Cellular and secreted proteins from BeWo cells were analyzed by Western blotting, and a band of about 22 kilodaltons was detected using a polyclonal antibody which cross-reacts with hGH-V and hCS. The level of 22 kilodalton band in samples of cellular as well as released protein was increased by T3 treatment. BeWo cells provide a model system for studying hGH-V and hCS regulation as well as tissue-specific expression.

Choriocarcinoma↗
PubMed1993

Ethanol alters hormone production in cultured human placental trophoblasts.

Maternal alcohol abuse during pregnancy can lead to abnormalities in fetal development, including the fetal alcohol syndrome (FAS). Although intrauterine growth retardation is a hallmark of FAS, the pathophysiology is not fully understood. A contributing factor may be altered placental function, which could affect fetal growth and development. As a major endocrine organ during pregnancy, changes in the production of placental hormones could affect pregnancy and possibly fetal development. In this study, the effect of continued exposure to ethanol on placental hormone production was examined using cultured human placental trophoblasts. Ethanol exposure involved diffusion of ethanol from the atmosphere into the culture medium. This was refreshed daily, leading to daily peak concentrations of 280 to 300 mg/dl (60-65 mM) at 16 to 24 hr. This ethanol exposure for 2 or 4 days significantly increased the production of human chorionic gonadotropin and progesterone by the cultured trophoblasts. However, ethanol treatment had no effect on human placental lactogen production. Acute stimulation (10 min) of cultured trophoblasts with adenosine (50 microM) normally results in increased production of cyclic adenosine 3',5'-monophosphate (cAMP). With ethanol exposure, adenosine-stimulated cAMP production was significantly elevated relative to that in controls. However, the effect of ethanol on adenosine-stimulated cAMP did not appear to be secondary to chronic alterations in adenosine in the culture medium. Measurement of adenosine in the culture medium revealed no difference in concentration or production between control and ethanol treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed2002

Placental growth hormone and lactogen production by perifused ovine placental explants: regulation by growth hormone-releasing hormone and glucose.

The factors controlling normal placental development are poorly understood. We have previously reported the presence of ovine placental growth hormone (oPGH) and growth hormone receptors in ovine placenta, and oPGH production by the trophectoderm and syncitium during the second month of pregnancy. To identify factors regulating oPGH production, we developed a perifusion system to measure oPGH and ovine placental lactogen (oPL) production by Day 45 ovine placental explants. The mRNAs for both hormones were quantitated by real-time polymerase chain reaction in explants collected after perifusion periods of up to 8 h. Ovine PGH and oPL were released into the medium at mean rates of 2.45 +/- 0.2 and 353.6 +/- 13.6 ng/g/h, respectively. Ovine placenta produces growth hormone-releasing hormone (GHRH), but addition of GHRH to the perifusion medium did not modify either oPGH or oPL production. In vivo, oPGH production occurs between Days 30 and 60 of pregnancy. Because modulation of the maternal diet during this period affects placental development, the potential regulation of oPGH and oPL production by glucose was evaluated. Glucose supplementation of the perifusion medium resulted in a concentration-dependent decrease in oPGH release after 4 h, but oPGH mRNA levels were not affected. Production of oPL was not affected by glucose. Thus, oPGH and oPL belong to the same growth hormone/prolactin family but are differentially regulated by glucose. Ovine PGH modulations should be taken into account in metabolic experiments performed during the first trimester of pregnancy in sheep.

Animals↗
PubMed1986

Variation among species in the endocrine control of mammary growth and function: the roles of prolactin, growth hormone, and placental lactogen.

Prolactin, growth hormone, and placental lactogen form a family of structurally related hormones, which may have evolved from a common ancestral peptide. Prolactin and growth hormone are present in all mammals, but the biological activity associated with placental lactogen has been detected in only some groups. Attempts to detect placental lactogen using bioassay and radioreceptor assay are reported and have been unsuccessful in an insectivore (the shrew), a bat, an edentate (the armadillo), a lagomorph (the rabbit), several carnivores (dog, cat, ferret), perissodactyls (horse, zebra, rhino), and, within the artiodactyls, pigs. Placental lactogenic activity has been detected in primates (chimpanzee, orangutan), rodents (voles, Pinon mouse, guinea-pig, mara), and in numerous artiodactyls (llama, giraffe, several species of deer, antelope, gnu, gazelle, musk ox, cape buffalo, Barbary sheep, several sheep of the genus Ovis, goat, and cow). These results confirm and extend the work of others and are discussed in relation to the evolution of these hormones. In synergism with steroid and thyroid hormones, protein hormones of the prolactin and growth hormone family play a crucial role in stimulating the development of the mammary gland, the differentiation and function of mammary cells to secrete milk, and in the systemic adjustments in maternal metabolism in pregnancy and lactation. Studies in vitro have shown that mammary tissues from several species synthesize milk components in response to insulin plus adrenal corticoid plus prolactin. However, there are also species differences in minimal hormonal requirements for lactogenesis. In vivo, for example, rabbits will initiate or sustain lactation in response to prolactin alone, whereas sheep and goats require prolactin plus growth hormone plus adrenal corticoid plus thyroid hormone. Measurement of hormone concentrations in the plasma of pregnant animals shows considerable differences among species in the pattern of secretion of lactogenic hormones to bring about mammary development. A surge of prolactin secretion occurs at parturition but may not be essential in the initiation of lactation. The timing of progesterone withdrawal correlates well with lactogenesis in eutherian mammals, but species differ in the mechanisms at parturition which bring this about. Marsupials show a quite different pattern of suckling-induced lactation. In maintaining lactation the greatest contrast is between ruminants, in which growth hormone is of particular importance, and other mammals, in which reduction of prolactin secretion with bromocriptine rapidly suppresses milk synthesis and secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Growth hormone binding protein and maternal body mass index in relation to placental growth hormone and insulin requirements during pregnancy in type 1 diabetic women.

In pregnancy, the growth hormone axis is shifted from pituitary growth hormone (GH) to placental growth hormone (PGH). Their common binding protein, GH binding protein (GHBP), displays peak serum levels at mid-gestation in normal individuals. In the non-pregnant state, diabetes is known to be associated with elevated levels of GH and decreased levels of insulin-like growth factors (IGFs) and GHBP. Diabetes in pregnancy may therefore as well be associated with disturbances in the growth hormone axis. In the present study, we aimed at investigating the impact of GHBP and maternal body mass index (BMI) on levels of PGH, thereby enabling estimation of any association between free PGH and weight adjusted insulin requirements. In 51 type 1 diabetic women, blood samples were collected in gestational week 10+, 16+, 22+, 28+ and 34+, and analysed for their serum content of GHBP, PGH, and GH. Serum GHBP increased from the first weeks of pregnancy to median 2.07 nmol/l (range 1.17-4.26) in week 22+, then declined to median 1.29 nmol/l (range 0.77-2.35) in week 34+ (ANOVA P < 0.001). Serum PGH levels were highest in week 34+ at median 21.3 microg/l (range 5.1-165.4) (P < 0.001), whereas a steady decrease in GH values was observed throughout pregnancy to a median 0.17 microg/l (range 0-5.53). The fraction of calculated free PGH to total PGH increased from mid-gestation onwards to 55.2% (37.0-87.1) in week 34+ at a median level of free PGH of 10.4 microg/l (range 1.9-144.0) (P < 0.001). Similarly, the molar ratio of total PGH to GHBP increased to a maximum of 0.68 (0.12-6.62) in week 34+. As in normal pregnancies, the correlation between BMI and GHBP was lost in late pregnancy. The newborns birth weight z-score correlated with total PGH and derivatives here-of in week 34+. Neither total nor weight adjusted insulin requirements correlated to total PGH, calculated free PGH, nor GHBP. In conclusion, PGH and GHBP display a similar course during pregnancy in type 1 diabetic women as described in normal women. The well-known association between GHBP and BMI was lost in late pregnancy. Calculated levels of free PGH were positively associated to fetal growth, but not to maternal insulin requirements.

Adult↗
PubMed2003

Increase in maternal placental growth hormone during pregnancy and disappearance during parturition in normal and growth hormone-deficient pregnancies.

OBJECTIVE: The purpose of this study was to evaluate placental growth hormone levels in maternal circulation throughout pregnancy in normal and growth hormone-deficient women with the use of a specific assay and to determine the clearance of placental growth hormone from maternal circulation after birth. STUDY DESIGN: Seventeen healthy pregnant women and 1 patient with growth hormone deficiency substituted with recombinant growth hormone during pregnancy participated in a longitudinal study from early pregnancy until birth with repetitive blood sampling and measurement of placental growth hormone levels throughout pregnancy. Furthermore, serial blood samples were drawn before, during, and after elective caesarean deliveries in 5 healthy women to calculate the half-life of placental growth hormone. Placental growth hormone was measured with the use of two monoclonal antibodies in a commercially available solid-phase iodine 125-labeled immunoradiometric assay (Biocode, Liège, Belgium). RESULTS: Placental growth hormone levels were detectable from as early as 8 weeks of gestation in some of the women and increased throughout gestation, with a maximum at approximately 35 to 36 weeks of gestation (13.7 ng/mL; range, 5.9-24.4 ng/mL) and large interindividual variations. Placental growth hormone levels did not correlate with birth weight or placental weight. In the patient with isolated growth hormone deficiency, placental growth hormone levels were detectable from 11 weeks of gestation (3.4 ng/mL) and increased throughout pregnancy to 13.9 ng/mL, which is similar to values that are obtained in the healthy pregnant women. Substitution therapy with recombinant human growth hormone did not suppress the increase in placental growth hormone. We found a mean half-life of placental growth hormone of 13.8 minutes (range, 11.5-15.2 minutes) in healthy pregnant women and an apparently similar half-life of placental growth hormone (15.8 minutes) in the growth hormone-deficient patient, assuming a monoexponential disappearance of placental growth hormone during the first 30 minutes after the delivery. After the initial 30 minutes, approximately 75% (range, 65%-89%) of the placental growth hormone had been cleared from the maternal circulation. CONCLUSION: Levels of placental growth hormone in maternal circulation increase throughout pregnancy from as early as 8 weeks of pregnancy, with maximum levels around the week 35 of gestation. The pregnancy-induced rise in placental growth hormone levels in the growth hormone-deficient patient was comparable to the rise seen during normal pregnancies and was not suppressed by the concurrent human growth hormone treatment. We speculate that maternal serum levels of placental growth hormone reflect placental function and fetal growth. However, further studies are needed to evaluate the potential clinical use of placental growth hormone determinations.

Adult↗
PubMed2002

Transcription factors underlying the development and endocrine functions of the placenta.

The placenta has been the subject of extensive basic research efforts in two distinct fields. The developmental biology of placenta has been studied because it is the first organ to develop during embryogenesis and because a number of different gene mutations in mice result in embryonic lethality due to placental defects. The trophoblast cell lineage is relatively simple such that only two major, terminally differentiated cell types appear: an "invasive trophoblast" cell subtype such as extravillous cytotrophoblast cells in humans and trophoblast giant cells in mice, and a "transport trophoblast" cell subtype that is a syncytium (syncytiotrophoblast) in humans and mice. These two cell types also have been the focus of endocrinologists because they are the source of major placental hormones. Understanding the transcriptional regulation of placental hormone genes has given insights into the control of specificity of gene expression. Because most placental hormones are produced by very specific trophoblast cell subtypes, the transcriptional details promise to give insights into cell-subtype specification. The fields of developmental biology and molecular endocrinology appear to be meeting on this common ground with the recent discovery of key transcription factors. Specifically, the basic helix-loop-helix (bHLH) transcription factor Hand1 is essential for differentiation of trophoblast giant cells in mice and also regulates the promoter for the giant cell-specific hormone, placental lactogen I gene (Pl1). In contrast, formation of syncytiotrophoblast cells in mice is controlled by a distinct genetic pathway that is governed by the Gcm1 transcription factor, a homologue of the Drosophila glial cells missing gene. Human GCM I has been shown to regulate the activity of the placental-specific enhancer of the aromatase gene (CYP19), which is specifically expressed in syncytiotrophoblast. Together, these findings imply that some key transcription factors have the dual functions of controlling both critical cell fate decisions in the trophoblast cell lineage and later the transcription of cell subtype-specific genes unrelated to development.

Animals↗
PubMed1989

Comparison of serum placental protein hormone levels in diabetic and normal pregnancy.

Conflicting data exist concerning maternal serum concentrations of placental hormones during pregnancy in women with diabetes mellitus. To resolve some of these discrepancies, women participating in the NICHD-Diabetes in Early Pregnancy Study were studied. In this collaborative study, pregnancy was identified within 21 days of conception by serum hCG measurements. We prospectively collected 185 blood samples from 35 insulin-dependent diabetic women and 166 blood samples from 31 control women, all between 5 and 37 weeks gestation. Serum concentrations of hCG, pregnancy-specific beta-1-glycoprotein, placental lactogen, and hCG alpha were measured serially. The relationship between serum hormone, fasting blood glucose, 1-h postprandial blood glucose, and glycosylated hemoglobin concentrations was compared. Serum hCG alpha levels were significantly lower in the diabetic women than in control women at multiple time points during the first and second trimesters, while no consistent differences in the serum concentrations of hCG or pregnancy-specific beta-1-glycoprotein were found between pregnant diabetic and control women. Serum placental lactogen levels were significantly lower in diabetic women at 9-10 weeks and 20 weeks gestation. There were no correlations between fasting blood glucose, 1-h postprandial blood glucose, or glycosylated hemoglobin and any of the placental protein levels in the diabetic women. These data are consistent with a defect in synthesis and/or secretion of hCG alpha by the cytotrophoblast during the first two trimesters of pregnancy in insulin-requiring diabetic women.

Adult↗
PubMed1997

Both pituitary and placental growth hormone transcripts are expressed in human peripheral blood mononuclear cells (PBMC).

The hGH-V gene codes for a variant of human pituitary growth hormone (hGH-N) named placental growth hormone (hPGH). hPGH shares 93% amino acid identity with hGH-N. Until now the hGH-V gene was considered to be exclusively expressed in human placenta, where it replaces maternal circulating hGH-N at the end of pregnancy. In this study we investigated by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis hGH-N, and hGH-V, gene expression in PBMC in men, women and pregnant women. We have demonstrated that hGH-N and hGH-V transcripts are simultaneously produced by PBMC in both men and women as well as pregnant women. The PBMC of a PIT-1-negative woman expressed only the hGH-V transcript, but not the hGH-N one as expected. In conclusion, hGH-V mRNA is expressed by cells other than the syncytiotrophoblast, is not regulated by PIT-1, and may be involved in immune regulation, as is pituitary GH.

Female↗