[Placental lactogen hormone and the oxytocin test. Comparison between 2 diagnostic methods for placental insufficiency].
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Adult↗
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Maternal serum placental growth hormone and insulinlike growth factor binding proteins 1 and 3 in pregnancies affected by fetal aneuploidy and other abnormalities: implications for prenatal diagnosis of trisomy 21.
In the present study, we determined circulating serum levels of human placental growth hormone (hPGH) and insulinlike growth factor binding proteins 1 and 3 (IGFBP-1 and IGFBP-3) using two-site radioimmunoassays during the gestational midtrimester of pregnancies affected by chromosomal disorders with the aim of identifying potential marker substances that might have a significant discriminative and predictive value for prenatal diagnosis of fetal chromosomal aberrations and of organ malformations such as neural-tube defect. Our results show that the maternal serum levels of hPGH were significantly elevated in pregnancies affected by chromosomal anomalies or organ malformations as compared with controls. The distribution of IGFBP-1 concentrations for all experimental groups except trisomy 21 were closely similar to the normal population. IGFBP-3 decreased slightly in pregnancies affected by Down syndrome. These findings suggest that hPGH may be useful as an additional marker in prenatal screening for Down syndrome.
Adolescent↗
Growth hormone and placental lactogen: biology, medicine and biotechnology.
Molecular cloning gave us access to the gene members of the human growth hormone and placental lactogen multigene family. Genomic sequencing provided clues for the understanding of the origin, functioning and regulation of this family. It has also allowed us to develop new diagnostic approaches for deficiencies of these hormones and to make new biotechnological contributions.
Evolution, Molecular↗
Somatogenic and lactogenic activity of the recombinant 22 kDa isoform of human placental growth hormone.
During pregnancy, the human placenta secretes a variant of pituitary growth hormone (hGH-V) differing in sequence from the pituitary growth hormone (hGH-N) by 13 amino acids substitutions. HGH-V replaces hGH-N in the maternal bloodstream during the second half of pregnancy. HGH-V is produced in two, possibly three, isoforms: a 22 kDa form, a glycosylated 25 kDa form, and a probable 26 kDa form resulting from alternative splicing of the mRNA. Here we have studied the somatogenic and lactogenic activity of recombinant 22 kDa hGH-V isoform produced in Escherichia coli and compared it with the 22 kDa form of hGH-N. The two variants exert a similar somatogenic effect on rabbit and rat cells, but differ as regards their lactogenic activity in the rat.
Alternative Splicing↗
Human placental lactogen hormone in serum from pregnant women with rhesus (anti-D) isoimmunization.
Determination of human placental lactogen hormone (HPL) was performed in 346 serum samples from 59 rhesus isoimmunized pregnant women. In all cases of fetal death-either intrauterine or in the first seven days after birth-we find a high level of HPL in maternal serum several weeks before death. All patients with normal HPL concentrations in the maternal serum, and who were treated by intrauterine transfusions, had surviving infants. If the indication for intrauterine transfusion is combined with an elevated HPL level in materal serum one must weigh the risk of the procedure against the poor prognosis for the fetus before deciding whether to intervene. Serum concentrations of human chorionic gonadotropin (HCG) and progesterone were of no clinical use, but we find a correlation between progesterone and HPL differing from the same correlation found in normal and diabetic pregnancies. A possible explanation is discussed in relation to the endoplasmic reticulum in the syncytiotrophoblast.
Blood Transfusion, Intrauterine↗
[Influence of placental protein hormones on maternal physiology].
Our data have demonstrated that maternal LH and FSH are repressed throughout pregnancy. Beside, we have discovered and characterized a variant placental GH. Our studies on the mechanism of anovulation and on pituitary GH suppression and GH physiology in pregnant women have contributed to demonstrate the autonomy of the fetoplacental unit and its effects on maternal anabolism and physiology. More specifically, human placental GH, coded by the GH-V gene appears responsible for the anabolic and somatotropic effects mediated by SM-C in the mother. The beneficial aspect of this mechanism for the species appears likely since placental tissues in which the GH-PL genes are deleted, express alternative gene(s) resulting in the production of a placental variant closely related or identical to pituitary 22K GH.
Chromosome Deletion↗
Molecular diagnosis of deletions in the human multigene complex of growth and placental lactogen hormones.
The type IA of the isolated deficiencies (ID) of growth (HGH) and placental lactogen (HPL) hormones are frequently the consequence of deletions in their respective genes. To facilitate the diagnosis of these cases, we developed a rapid method for detecting deletions of the genes involved based on the polymerase chain reaction (PCR) technique. This method consist of the simultaneous amplification via consensus primers of the 5 genes which conform the hGH-hPL multigene family, followed by the identification of each of them in the amplification product by gene-specific patterns of restriction enzyme cuts evidenced by agarose gel electrophoresis. We demonstrate the effectiveness of our method by identifying patients with deletions in gene members of the hGH-hPL family.
Adolescent↗
Degradation of parathyroid hormone by placental homogenate.
Degradation of the bovine parathyroid hormone (PTH) fragment (amino acids 35-84) up to 70% was observed during passage through human placenta in an in vitro perfusion model. Fractionation of the subcellular fractions of human placental homogenate revealed the degradation to take place only in the mitochondrial fraction. It is concluded that human placenta, like kidney and liver, has the ability to degrade PTH.
Female↗
Expression of insulin-like growth factor-I and placental growth hormone mRNA in placentae: a comparison between normal and intrauterine growth retardation pregnancies.
Intrauterine growth restriction (IUGR) is generally defined as the pathological restriction of fetal growth resulting in a fetus with birth weight below the 10th percentile for gestational age. Almost 75% of IUGR cases develop during third trimester. Studies on animals (rodents and sheep) as well as humans suggest that insulin-like growth factor-I (IGF-I), under the influence of placental growth hormone (PGH) plays crucial roles in fetal growth regulation during this period. Limited data are available with regard to IGF-I and PGH in placentae of normal and IUGR births. Therefore, in the present study, IGF-I and PGH mRNA expression has been studied in term placentae of normal (n = 10) and IUGR (n = 15) births by in-situ hybridization procedure. Their expression was also studied in first (n = 5) and second (n = 5) trimester placentae obtained from elective termination of normal pregnancies. Both IGF-I and PGH expression were found to be higher in the first and second trimester placentae compared to term placentae in normal pregnancies. However, IUGR term placentae showed increased expression of both IGF-I and PGH mRNA in comparison with normal placentae. Various mechanisms leading to the increased transcription of IGF-I and PGH mRNA in IUGR placenta are discussed. This increased transcription perhaps occurs in response to the reduction in the fetal growth.
Female↗
Placental steroid hormone biosynthesis in primate pregnancy.
Substantial advances in our understanding of placental function have resulted from recent establishment of in vitro approaches, such as cell culture, and application of molecular methods to study placental steroidogenesis. Insight into the processes of placental cell differentiation and hormonal function has been gained from culture of relatively pure preparations of cytotrophoblast. Various factors, e.g. cAMP and peptide growth factors, have been shown to have striking effects on progesterone and estrogen formation by placental tissue under in vitro conditions. Using advanced molecular approaches, the genes governing specific enzymes critical to placental steroidogenesis have been identified. Regulation of the mRNAs encoding specific enzyme peptides and thus expression of the genes by factors, such as cAMP, have been elucidated by Northern analysis and other techniques. It is critical that these contemporary approaches continue to be implemented aggressively to further elucidate placental function. However, it is clear from a survey of the literature, particularly of the past decade, that the vast majority of investigation in the area has been conducted in vitro. It is essential to determine whether the factors that have been observed to regulate placental endocrine function in vitro are operable in vivo. It is only with in vivo study that the dynamics of steroidogenesis and the complex functional relationships between placenta, fetus, and mother will be uncovered and understood. It is increasingly evident that the regulation of placental steroidogenesis involves autocrine and/or paracrine mechanisms, similar to those integral to hormone biosynthesis within other reproductive organs, e.g. ovary and testis. For example, as discussed above, estrogen regulates LDL uptake and P-450scc, and thus apparently is involved in generating substrate for progesterone production within the placenta. Conversely, progesterone has effects on 17 beta-hydroxysteroid oxidoreductase and thus the metabolism of estradiol, while androgens exert marked inhibitory effects on placental progesterone formation, at least in vitro. Not surprisingly, the regulation of placental progesterone and estrogen formation also is multifactorial. Thus, aromatase activity is stimulated synergistically by cAMP and phorbol esters, an effect that is suppressed by peptide growth factors. Therefore, the autocrine/paracrine and multifactorial regulation of hormone biosynthesis that has been relatively well documented in other tissues should be recognized as important in the primate placenta. Finally, the basic mechanisms underlying regulation of steroidogenesis within the fetoplacental unit during primate pregnancy appear similar, in important ways, to those of widely used laboratory animals, such as the rat and rabbit.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Placental prolactins and the physiology of pregnancy.
Mammalian pregnancy is characterized by a concerted and widespread series of changes in maternal physiology, many of which are direct responses to the binding of placental hormones to maternal targets. Among these placental hormones are proteins closely related to prolactin. In rodents, a large number of these placental prolactin-related hormones are expressed that have a broad spectrum of activities, including activities on endothelial cells and blood cells.
Animals↗
Placental and ovarian hormones in anembryonic pregnancy.
The circulating levels of human chorionic gonadotrophin (HCG), pregnancy-associated plasma protein-A (PAPP-A), Schwangerschaft protein 1 (SP-1), oestradiol and progesterone were measured in 81 pregnant patients between 4 and 11 weeks gestation, following in-vitro fertilization and embryo transfer. The patients were divided as follows: singleton anembryonic pregnancies, n = 22; singleton pregnancies which spontaneously aborted following the demonstration of fetal heart activity, n = 7; and normal singleton pregnancies, n = 52. The levels of all substances measured were significantly reduced in women with anembryonic compared to those with singleton pregnancies which proceeded to term. The serum levels of SP-1, weeks 6-8 (P < 0.01); HCG, weeks 6-8 (P < 0.05); oestradiol, weeks 5-8 (P < 0.05) and progesterone, weeks 6-8 (P < 0.05), were lower in anembryonic pregnancies than in those of pregnancies which spontaneously aborted. These differences may be a reflection of the fact that miscarriage, after the demonstration of fetal heart activity, represents fetal demise at a later stage in pregnancy. In anembryonic pregnancies, significant associations were found between HCG and both oestradiol and progesterone levels from weeks 6 and 8, suggesting that in the absence of an embryo, HCG is the prime determinant of steroid synthesis by the corpus luteum.
Abortion, Spontaneous↗
[Introduction to obstetrical endocrinology. 15. Placental steroid hormones].
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Chemical Phenomena↗
Effects of bovine growth hormone, human placental lactogen and ovine prolactin on intestinal fluid and ion transport in the rat.
The influence of bovine growth hormone and human placental lactogen on intestinal absorption was compared with that of ovine prolactin. Administration of each of these hormones in vivo daily for 2 days, resulted in increased fluid and electrolyte transport by the rat intestine, as measured in vitro. Hypophysectomy causes a fall in fluid and ion absorption in the rat jejunum but these changes are prevented by growth hormone treatment. Bovine growth hormone and ovine prolactin produce essentially similar effects in intact rats: significant increases in fluid, sodium and calcium transport in the duodenum; in fluid, sodium and potassium transport in the jejunum; in sodium, chloride, potassium and calcium transport in the ileum. Growth hormone also significantly increased fluid, sodium and chloride transport in the colon. Treatment of hypophysectomized rats with human placental lactogen enhanced fluid and ion transport in the jejunum; however, it failed to restore normal potassium transport in the ileum and colon at the 1 mg daily dose level. Growth hormone and human placental lactogen appear to affect jejunal water and electrolyte transport in the same manner as occurs with prolactin, possibly by influencing active ion transport.
Animals↗
[Choriogonadotrophic hormone and placental tumors].
The radioimmunological dosage of choriogonadotrophic hormone is the actual basis for the choice of patients to be treated, to recognize the poor prognosis cases, to adjust the treatment in drugs, doses and durations, to detect the relapses. The clinicien must obey the biologist who is always right.
Antineoplastic Agents↗
Analysis of placental regulation of hematopoiesis.
Placental hormones contribute to changes in maternal physiology, especially to changes in the blood system. Methods are described to express a placental hormone from a cloned cDNA by transfection into a mammalian cell line, to purify the hormone, and to assess the activities of the hormone in primary mouse bone marrow cell cultures. The example used in this chapter is prolactin-like protein F (PLP-F), a recently discovered mouse placental hormone that acts on the myeloid lineage. This hormone has been expressed at high levels in stably transfected Chinese hamster ovary cells. The protein is secreted from these cells after cleavage of the signal sequence and the addition of N-linked carbohydrate. A series of chromatographic steps are used to purify the protein to homogeneity, which is verified by gel electrophoresis and silver staining; the identity of the purified protein is confirmed by immunoblot analysis. Purified protein is then assayed by addition to primary bone marrow cells and scoring the growth and the differentiation of the megakaryocyte progenitor, colony forming unit-megakaryocyte.
Animals↗
Detection of placental growth hormone variant and chorionic somatomammotropin-L RNA expression in normal and diabetic pregnancy by reverse transcriptase-polymerase chain reaction.
Diabetes is a common complication encountered during pregnancy. Earlier studies indicated that diabetic placentas bear morphological alterations consistent with modified placental differentiation, including alterations in the villous cellular content, structure, and total surface. Limited data associating the diabetic status with the expression of terminal placental differentiation markers are available. The human growth hormone/chorionic somatomammotropin (hGH/CS) family consists of five genes, one of which (GH-N) is expressed efficiently in pituitary while the other four (CS-A, B, L, and hGH-V) are expressed in placenta and represent ultimate placental differentiation markers. We developed and applied a sensitive RT-PCR method coupled with diagnostic restriction digestion to determine the relative levels of the hGH/CS family in normal pregnancies and examine whether their mRNA expression pattern is altered in pregnancies complicated by diabetes. We show that relative hCS-L content changes during placental development. Specifically, normal term placentas express higher relative levels of hCS-L, lower relative hGH-V levels and a 70-fold lower hGH-V/CS-L mRNA ratio compared to early placentas. Also, many term placentas from diabetic pregnancies express lower relative levels of hCS-L mRNA and a much higher hGH-V/CS-L mRNA ratio compared to normal term placenta, resembling more an early placenta pattern of expression. Thus, our study suggests that the expression of terminal placental differentiation markers, such as the hGH/CS genes, is altered in term placentas from these diabetics reflecting either impaired placental differentiation or post-differentiation impairment of normal placental function.
Diabetes, Gestational↗
Processing of placental peptide hormones synthesized in lysates containing membranes derived from tunicamycin-treated ascites tumor cells.
To examine the relationship between pre-protein cleavage and nascent chain glycosylation placental mRNA was translated in a reconstituted ascites cell-free system containing microsomal membranes prepared from tunicamycin-treated or untreated ascites tumor cells. In the absence of membranes, first trimester RNA directed the synthesis of the pre-form of the alpha subunit of human chorionic gonadotropin, whereas, in the presence of normal membranes, first trimester RNA directed the synthesis of a glycosylated form of the alpha subunit. Cell-free lysates containing membranes derived from tunicamycin-treated cells synthesized an alpha subunit protein with little, if any, carbohydrate. This protein was apparently sequestered into membranes since it was resistant to the action of trypsin which was added after translation. The pre-peptide of the alpha subunit protein was removed by treated membranes as determined by amino acid sequence analyses. The non-glycosylated protein pre-placental lactogen was also cleaved to its mature form by tunicamycin membranes. These data strongly suggest that, in vitro, glycosylation is not obligatory for pre-protein cleavage and sequestration of these placental protein hormones.
Animals↗