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Biology of Reproduction Mar 2002The factors controlling normal placental development are poorly understood. We have previously reported the presence of ovine placental growth hormone (oPGH) and growth...
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.
Topics: Animals; Female; Gene Expression Regulation; Glucose; Growth Hormone; Growth Hormone-Releasing Hormone; In Vitro Techniques; Placenta; Placental Hormones; Placental Lactogen; Polymerase Chain Reaction; Pregnancy; RNA, Messenger; Sheep; Time Factors
PubMed: 11870057
DOI: 10.1095/biolreprod66.3.555 -
International Journal of Molecular... Jul 2021Human placentation differs from that of other mammals. A suite of characteristics is shared with haplorrhine primates, including early development of the embryonic... (Review)
Review
Human placentation differs from that of other mammals. A suite of characteristics is shared with haplorrhine primates, including early development of the embryonic membranes and placental hormones such as chorionic gonadotrophin and placental lactogen. A comparable architecture of the intervillous space is found only in Old World monkeys and apes. The routes of trophoblast invasion and the precise role of extravillous trophoblast in uterine artery transformation is similar in chimpanzee and gorilla. Extended parental care is shared with the great apes, and though human babies are rather helpless at birth, they are well developed (precocial) in other respects. Primates and rodents last shared a common ancestor in the Cretaceous period, and their placentation has evolved independently for some 80 million years. This is reflected in many aspects of their placentation. Some apparent resemblances such as interstitial implantation and placental lactogens are the result of convergent evolution. For rodent models such as the mouse, the differences are compounded by short gestations leading to the delivery of poorly developed (altricial) young.
Topics: Animals; Biological Evolution; Female; Humans; Placenta; Placental Hormones; Placentation; Pregnancy; Primates; Uterine Artery
PubMed: 34360862
DOI: 10.3390/ijms22158099 -
Anales Espanoles de Pediatria Jun 1992
Review
Topics: Animals; Blotting, Western; Female; Growth Hormone; Humans; Infant, Newborn; Placental Hormones; Pregnancy; Pregnancy Proteins; Pregnancy Trimester, Third; Rats; Receptors, Somatotropin
PubMed: 1416510
DOI: No ID Found -
Placenta Feb 2012Evolutionary genetic arguments suggest that pregnancy is not a fully cooperative engagement between the mother and embryo. Trivers' concept of parent-offspring conflict... (Review)
Review
Evolutionary genetic arguments suggest that pregnancy is not a fully cooperative engagement between the mother and embryo. Trivers' concept of parent-offspring conflict indicates that the mother and embryo will disagree over the level of maternal investment in the pregnancy. Therefore, selection will favour mechanisms encoded by maternal genes that limit resource transfer to the embryo and mechanisms encoded by embryonic genes that enhance such transfer. These antagonistic selection pressures may have influenced the evolution of many aspects of placental regulation and function, including genomic imprinting and placental hormone production. However, the mother and embryo are not expected to disagree over aspects of placental function that benefit both parties; for example, regulation of haemostasis or resistance to infections etc. Therefore, an understanding of the complex regulation of placental function must consider the multiple selection pressures acting on this organ.
Topics: Adaptation, Physiological; Altruism; Animals; Behavior, Animal; Conflict, Psychological; Epigenesis, Genetic; Female; Genomic Imprinting; Humans; Male; Parent-Child Relations; Placenta; Placental Hormones; Pregnancy; Reproductive Behavior; Selection, Genetic; Sexual Behavior, Animal; Social Behavior; Stress, Psychological
PubMed: 22153682
DOI: 10.1016/j.placenta.2011.11.016 -
Contributions To Gynecology and... 1991
Review
Topics: Adrenocorticotropic Hormone; Chorionic Gonadotropin; Female; Humans; Placenta; Placental Hormones; Pregnancy; beta-Endorphin
PubMed: 1657522
DOI: No ID Found -
Placental growth hormone is increased in the maternal and fetal serum of patients with preeclampsia.The Journal of Maternal-fetal &... Sep 2007Placental growth hormone (PGH) is a pregnancy-specific protein produced by syncytiotrophoblast and extravillous cytotrophoblast. No other cells have been reported to...
OBJECTIVES
Placental growth hormone (PGH) is a pregnancy-specific protein produced by syncytiotrophoblast and extravillous cytotrophoblast. No other cells have been reported to synthesize PGH Maternal. PGH Serum concentration increases with advancing gestational age, while quickly decreasing after delivery of the placenta. The biological properties of PGH include somatogenic, lactogenic, and lipolytic functions. The purpose of this study was to determine whether the maternal serum concentrations of PGH change in women with preeclampsia (PE), women with PE who deliver a small for gestational age neonate (PE + SGA), and those with SGA alone.
STUDY DESIGN
This cross-sectional study included maternal serum from normal pregnant women (n = 61), patients with severe PE (n = 48), PE + SGA (n = 30), and SGA alone (n = 41). Fetal cord blood from uncomplicated pregnancies (n = 16) and PE (n = 16) was also analyzed. PGH concentrations were measured by ELISA. Non-parametric statistics were used for analysis.
RESULTS
(1) Women with severe PE had a median serum concentration of PGH higher than normal pregnant women (PE: median 23,076 pg/mL (3473-94 256) vs. normal pregnancy: median 12 157 pg/mL (2617-34 016); p < 0.05), pregnant women who delivered an SGA neonate (SGA: median 10 206 pg/mL (1816-34 705); p < 0.05), as well as pregnant patients with PE and SGA (PE + SGA: median 11 027 pg/mL (1232-61 702); p < 0.05). (2) No significant differences were observed in the median maternal serum concentration of PGH among pregnant women with PE and SGA, SGA alone, and normal pregnancy (p > 0.05). (3) Compared to those of the control group, the median umbilical serum concentration of PGH was significantly higher in newborns of preeclamptic women (PE: median 356.1 pg/mL (72.6-20 946), normal pregnancy: median 128.5 pg/mL (21.6-255.9); p < 0.01). (4) PGH was detected in all samples of cord blood.
CONCLUSIONS
(1) PE is associated with higher median concentrations of PGH in both the maternal and fetal circulation compared to normal pregnancy. (2) Patients with PE + SGA had lower maternal serum concentrations of PGH than preeclamptic patients without SGA. (3) Contrary to previous findings, PGH was detectable in the fetal circulation. The observations reported herein are novel and suggest that PGH may play a role in the mechanisms of disease in preeclampsia and fetal growth restriction.
Topics: Adolescent; Adult; Cross-Sectional Studies; Female; Fetal Blood; Fetal Growth Retardation; Fetal Weight; Growth Hormone; Humans; Infant, Newborn; Mothers; Placental Hormones; Pre-Eclampsia; Pregnancy
PubMed: 17701665
DOI: 10.1080/14767050701463571 -
Experimental and Clinical Endocrinology 1994Removal of the pituitary from pregnant rats provided early evidence that the placenta was the source of prolactin-like bioactivity. After mid-pregnancy the placenta was... (Comparative Study)
Comparative Study Review
Removal of the pituitary from pregnant rats provided early evidence that the placenta was the source of prolactin-like bioactivity. After mid-pregnancy the placenta was able to support progesterone production by the corpus luteum (luteotrophic activity) and continued development of the mammary gland (mammotrophic activity). Three groups of mammals, the rodents, the ruminant artiodactyls and the primates are now known to produce from fetal placenta a remarkable variety of proteins which are related in structure to pituitary prolactin and growth hormone. Prolactin and growth hormone are themselves structurally related and are thought to have arisen from a common ancestral gene by gene duplication and evolutionary divergence. The receptors with which they interact also form a family of homologous proteins. Surprisingly the placental lactogens appear to have arisen more than once in evolution since in primates they are structurally closely related to growth hormone, while in rodents and ruminants they have closer similarity to prolactin. There is suggestive evidence that there may be specific receptors for placental lactogens in some fetal and maternal tissues. In humans a five-gene cluster on chromosome 17 contains two growth hormone (GH) and three placental lactogen (PL) genes. Two human PL genes encode identical proteins that are expressed in the placenta. One of the human GH genes is also placentally expressed. In mice, chromosome 13 carries the genes for mouse prolactin, for placental lactogen-I and -II (PL-I and PL-II) and for two other prolactin-related proteins, the proliferins. Rats also express PL-I and PL-II, together with at least three other placental prolactin-like proteins different from proliferins.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Animals; Growth Hormone; Humans; Mice; Multigene Family; Placental Hormones; Prolactin; Rats; Receptors, Peptide; Ruminants; Species Specificity; Structure-Activity Relationship
PubMed: 7995346
DOI: 10.1055/s-0029-1211288 -
The Journal of Clinical Endocrinology... May 2010
Topics: Birth Weight; Child; Diabetes Mellitus, Type 2; Female; Fetal Development; Growth Hormone; Humans; Infant, Low Birth Weight; Infant, Newborn; Placenta; Placental Hormones; Placental Lactogen; Pregnancy; Prolactin; Weight Gain
PubMed: 20444932
DOI: 10.1210/jc.2010-0517 -
Endokrynologia Polska 2013In the search for biomarkers that allow the prediction of neonatal growth and development, placental growth hormone(PGH), pituitary growth hormone (GH1), insulin-like... (Comparative Study)
Comparative Study
INTRODUCTION
In the search for biomarkers that allow the prediction of neonatal growth and development, placental growth hormone(PGH), pituitary growth hormone (GH1), insulin-like growth factor 1 (IGF-1), and ghrelin concentrations were assessed in the amniotic fluid and in the umbilical cord blood of 92 neonates.
MATERIAL AND METHODS
The proteins were assayed by the ELISA method. Their concentration values were compared in 57 full-term neonates and 35 prematurely born neonates, as well as in both large (> 4,000 g) and small neonates (< 2,500 g). Also, body mass and placenta mass were compared.
RESULTS
Statistically significant differences both between prematurely born neonates and full-term neonates and between large and small neonates were obtained only in terms of the body mass of neonates and placenta mass. The concentration values of the hormones studied did not show statistically significant differences. A distinct tendency was noticed towards an increase in PGH concentration in both prematurely born and small neonates. In large neonates, statistically significantly higher IGF-1 concentrations were found compared to the prematurely born neonates.
CONCLUSIONS
Our studies indicate an important role for PGH in maintaining a proper IGF-1 pool and demonstrate the existence of a direct influence on the function of the placenta in prematurely born neonates through the activation of compensation mechanisms,which stimulate IGF-1 synthesis.
Topics: Amniotic Fluid; Biomarkers; Birth Weight; Enzyme-Linked Immunosorbent Assay; Female; Fetal Blood; Ghrelin; Growth Hormone; Humans; Insulin-Like Growth Factor I; Placenta; Placental Hormones; Pregnancy
PubMed: 24002957
DOI: 10.5603/ep.2013.0008 -
Molecular and Cellular Endocrinology Apr 2011Perfluorooctanoic acid (PFOA) is a persistent pollutant worldwide and even found in human cord blood and breast milk. Some animal studies have reported that PFOA causes...
Perfluorooctanoic acid (PFOA) is a persistent pollutant worldwide and even found in human cord blood and breast milk. Some animal studies have reported that PFOA causes developmental toxicity such as fetal weight loss, but the mechanism is still unclear. This study focused on developmental toxicity of PFOA, particularly impacts of PFOA on placental endocrine function such as placental prolactin (PRL)-family hormone gene expression and fetal growth in mouse. Time-mated CD-1 mice were dosed by gavage with 0, 2, 10 and 25 mg/kg B.W/day of PFOA (n-10) dissolved with de-ionized water from gestational day (GD) 11-16. During treatment, body weight of each pregnant mouse was measured daily. On day 16, caesarean sections were performed and developmental data were observed. Three placentas from three different pregnant mice were assigned to each of the following experiments. The mRNA levels of mouse placental lactogen (mPL)-II, prolactin like protein (mPLP)-E, -F and Pit-1α and β isotype mRNAs, a transacting factor of mPLs and mPLPs genes, were analyzed using northern blot, in situ hybridization and RT-PCR, respectively. Maternal body weight gain was significantly declined from GD 13 in the PFOA treated groups compared to control. Developmental data such as fetal and placental weights were significantly decreased in accordance with PFOA dosage. Number of dead fetuses and post-implantation losses were significantly increased in the PFOA-exposed groups. In addition, placental efficiency (fetal weight/placental weight) was significantly reduced in PFOA treated groups in accordance with PFOA dosage. Histopathologic changes were observed in placenta. Dose dependent necrotic changes were observed in both 10 mg and 25 mg PFOA treated groups. Cell frequency of glycogen trophoblast cell and parietal trophoblast giant cell were decreased dose dependently in the junctional zone. In the labyrinth zone, sinusoidal trophoblast giant cell frequency was decreased in the 25 mg PFOA treated group. Also, morphological change such as crushed nuclear (atrophy) of trophoblast cells was observed in 25 mg PFOA treated group. Finally, mRNA levels of the mPL-II, mPLP-E, -F and Pit-1α and β were significantly reduced in the PFOA treated groups dose dependently. In addition, the changing pattern between mPL-II, mPLP-E, -F mRNA levels and fetal body weight showed positive relationship. In conclusion, the inhibitory effects of PFOA on the placental prolactin-family hormone genes expression may be secondary effects to insufficient trophoblast cell type differentiation and/or increased trophoblast cell necrosis. The impacts of PFOA on placental development and endocrine function reduced the placental efficiency and partly contributed to the fetal growth retardation in the mouse.
Topics: Animals; Body Weight; Caprylates; Cell Count; Cytokines; Female; Fetal Death; Fetal Growth Retardation; Fetal Weight; Fluorocarbons; Mice; Placenta; Placental Hormones; Placental Lactogen; Pregnancy; Pregnancy Proteins; Transcription Factor Pit-1; Transcription, Genetic; Trophoblasts
PubMed: 21241770
DOI: 10.1016/j.mce.2011.01.009