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PubMed1998

Structural and molecular studies of human chorionic gonadotropin and its receptor.

Human chorionic gonadotropin (hCG) is a placental hormone that stimulates secretion of the pregnancy-sustaining steroid progesterone. It and other glycoprotein hormones are disulfide-rich heterodimers that share a common alpha chain and distinctive beta chains specific to their particular G protein-linked receptors. We determined the structure of partially deglycosylated hCG at 2.6 A resolution from multiwavelength anomalous diffraction (MAD) measurements of a selenomethionyl hCG crystal. We have also begun three- and four-dimensional structural studies on the biologically active hormone and have determined the structure of the carbohydrate attached to the alpha-subunit. Despite little sequence similarity limited to 10% identity, the alpha and beta subunits of hCG maintain strikingly similar tertiary folds, with cystine-knot motifs at cores of extended hairpin loops. Structural and sequence comparisons indicate an evolutionary homology between the glycoprotein hormone chains and other cystine-knot proteins, notably PDGF, TGF-beta, and NGF. This structural similarity has led us to speculate that early hCG secretion has a broader role than solely the stimulation of the corpus luteum; indeed, levels of hCG, which rise rapidly in the circulation after implantation, are greater than the levels necessary for corpus luteum function. One such role of hCG or its subunits could be as a growth factor that facilitates endometrial receptivity. Our studies of hCG have also identified structural variants, notably in the carbohydrate moiety, that are distinctive for patients with a variety of disorders of pregnancy, including hydatidiform mole and choriocarcinoma. We have also focused our efforts on using information gleaned from the structure of hCG for the design of drug-like molecules that might serve as either agonists or antagonists of hCG. To facilitate these experiments, we have designed a rapid screen for the identification of molecules that might bind the hCG receptor by identifying compounds that disrupt binding of hCG to its receptor. This screen employs a filamentous phage that displays the extracellular domain of the hCG receptor on its surface. Thus far, we have identified a few compounds that disrupt binding of hCG with its receptor at a concentration of approximately 1 micromolar. These "lead" molecules are currently being modified in an attempt to identify a molecule that can disrupt binding of hCG at nanomolar concentrations.

Amino Acid Sequence↗
PubMed1985

Placental protein and hormone measurements in twin pregnancy.

Maternal serum levels of human placental lactogen (hPL), schwangerschaftsprotein 1 (SP1), pregnancy-associated plasma protein A (PAPP-A), placental protein 5 (PP5) and total oestriol (E3) were measured serially in 35 twin pregnancies during the third trimester. Eighteen pregnancies had major complications including dysmaturity of one or both fetuses in nine, premature labour in six, and placental abruption in three. Serum levels of all five variables were higher than in singletons, this distinction being greatest for hPL and lowest for SP1 and E3. The levels of hPL, PP5 and E3 just before delivery were significantly correlated with the total birthweight, a correlation with placental weight being evident only for hPL and PP5. A significant correlation between the five biochemical variables at 33-34 weeks was only seen between hPL and PAPP-A. Protein and hormone levels in the abnormal twin pregnancies were not apparently different from those in the normal twin pregnancies. These data suggest that only hPL levels biochemically reflect this extreme of fetal and placental growth, but that neither the levels of hPL nor any of the other biochemical indices examined are altered in abnormalities in twin pregnancy.

Birth Weight↗
PubMed2002

Intracellular signaling by growth hormone variant (GH-V).

Placental growth hormone, or growth hormone variant (GH-V), is a member of the growth hormone gene family. Its physiologic role during pregnancy remains undefined. Although extensive work has been done characterizing the signaling pathways activated by hGH, the signaling pathways which are activated by GH-V have not been characterized. We investigated cellular signaling by GH-V in model systems in which signaling by hGH has been well characterized. GH-V activates the STAT5b transcription factor in the IM-9 human lymphocyte and 3T3-F442A preadipocyte cell lines, and in primary porcine smooth muscle cells, which all homologously express GH receptors. In contrast, hCS does not activate signaling in these GH receptor-expressing cells. Like hGH, signaling by GH-V is inhibited by the GH antagonist (G120K). These results provide preliminary evidence that GH-V plays a major role in affecting target cells expressing the GH receptor, thus potentially exerting significant GH-like effects on maternal physiology during pregnancy.

3T3 Cells↗
PubMed1982

Placental and serum hormone changes during the second half of pregnancy in the hamster.

The concentrations of androgen, estrogen, progesterone, and prolactin-like hormones in serum, placentae, and media from placental incubations during the second half of pregnancy in the hamster were determined. Concentrations of prolactin-like activity in serum, placentae, and media from placental incubations increased from Day 8 to Day 14 of gestation. On Day 16 of pregnancy the content and in vitro release of placental prolactin-like activity declined; however, serum prolactin-like activity increased. The in vitro release of 3H-protein by hamster placentae showed gestational changes resembling the pattern of in vitro placental lactogen release. Serum and placental content of progesterone increased from Day 8 to Day 14 of gestation and declined from Day 14 to Day 16. In vitro placental progesterone release increased from Day 8 to Day 12 and declined from Day 12 to Day 16. Serum estrogen levels were elevated during the second half of pregnancy, whereas serum androgen levels were minimal. Neither estrogen nor androgen production by hamster placentae could be detected.

Androgens↗
PubMed1999

Placental corticotropin-releasing hormone: function and regulation.

Corticotropin-releasing hormone is a neuropeptide placentally expressed among mammals only in primates. Its expression increases as much as 100 times during the last 6 to 8 weeks of pregnancy and is paradoxically stimulated by glucocorticoids. Increasing evidence suggests that placental corticotropin-releasing hormone may have evolved in primates to stimulate fetal adrenocorticotropin release and adrenal steroidogenesis, thus satisfying the high demand for synthesis of dehydroepiandrosterone, the predominant source of placental estradiol. Concomitant stimulation by placental corticotropin-releasing hormone of fetal cortisol and dehydroepiandrosterone would couple the glucocorticoid effects on fetal organ maturation with the timing of parturition, an obvious benefit in postnatal survival.

Animals↗
PubMed1989

[Growth hormone, insulin and placental lactogen in the sera of mothers and fetal blood of infants from physiological pregnancy and pregnancy complicated by diabetes mellitus].

The study was aimed at investigating the changes in the blood serum concentrations of growth hormone (HGH), insulin and placental lactogen (HPL) in the newborns of diabetic mothers as compared to those born from physiological pregnancies. The concentration of hormones was determined by RIA both in the newborns and in mothers of the two groups. The mean insulin concentration was significantly higher, and that of HGH significantly lower in the newborns of diabetic mothers, as compared to those of healthy mothers. It seems that the occurrence of fetal macrosomy in diabetic pregnancies is associated with high insulin levels.

Female↗
PubMed1983

Effects of hypophyseal, placental, hypophysiotropic, and steroid hormones on ovipositor elongation and ovulation in the rose bitterling, Rhodeus ocellatus ocellatus.

Effects of various hypophyseal, placental, hypophysiotropic, and steroid hormones on ovipositor elongation and ovulation were investigated using the mature female rose bitterling, Rhodeus ocellatus ocellatus. Mammalian LH and HCG were effective at high doses whereas mammalian prolactin, FSH, ACTH, TSH, and neurohypophyseal hormones were ineffective. Synthetic LH-RH had some effects at very high doses. Fish pituitary extracts were much more potent than mammalian gonadotropins and a dose-response curve of elongation was obtained. This suggests that the ovipositor test is a good bioassay for fish gonadotropin. Some C21-steroids, especially 17 alpha-hydroxyprogesterone and 17 alpha-hydroxy-20 beta-dihydroprogesterone, also had prominent effects on ovipositor elongation, indicating the effects of gonadotropins may be via some C21-steroids. Hypophysectomy did not affect the sensitivity to gonadotropin but somewhat reduced the response to steroid. The relationship between the activity of steroids and their structure is discussed.

Animals↗
PubMed2006

Hormonal regulation of placental nitric oxide and pathogenesis of pre-eclampsia.

The placenta is central to foetal growth and development in mammalian pregnancy. Compromised placental function (as found in pre-eclampsia) often results in life-threatening situations for both mother and foetus. The nitric-oxide (NO) signalling cascade is important for placental function, in particular for the development of the vascular network and for maintaining vascular tone. This pathway seems to be regulated by multiple hormonal signals. Emerging evidence suggests that pathogenic mechanisms that are involved in abnormal placental function target specific molecules, such as hormone receptors, that regulate NO release and have subsequent dramatic consequences. Here, we discuss the current knowledge of NO function in the placenta, its hormonal regulation in normal pregnancy and in the pathophysiology of pre-eclampsia, its potential pathogenic mechanisms and possible use as a therapeutic target.

Animals↗
PubMed1988

Secretion of corticotropin-releasing hormone by superfused human placental fragments.

Corticotropin-releasing hormone (CRH) immunoreactivity (IR) is present in the blood of women in the 3rd trimester of pregnancy and in placental extracts. We have used a placental fragment superfusion system to investigate the release of CRH from fresh placental tissue. Fragments of normal term placenta were mixed with Biogel P2, packed into minicolumns and superfused with carbogen-gassed Earles buffer at 37 degrees C. The rheology of the superfusion system was determined and the oxygen consumption of the superfused placental fragments indicated viability of the tissue preparation over a 5-hour time span. CRH IR in the eluate was measured by radioimmunoassay (RIA) using the 41 residue synthetic peptide human, rat CRH-41 (h, r CRH-41) as the standard, 125I labelled Tyr- h, r CRH as the tracer and rabbit anti-ovine CRH as the antibody. The sensitivity of the assay is 2 pM. Size exclusion chromatography on Sephadex G-50 of the placental column eluate displayed one major peak of CRH IR which co-eluted with that of h, r CRH. Placental fragment superfusate displayed potent CRH bioactivity as assessed by beta-endorphin secretion from ovine pituitary cells. Replacing the superfusing medium of the placental fragments with 45 mM KCl resulted in a prompt increase in the release of CRH IR. These results indicate that placental cells in vitro secrete a molecule of similar molecular weight, immunoreactivity and bioactivity to h, r CRH and that the rate of secretion may be regulated.

Animals↗
PubMed1991

Differential binding of rat pituitary-specific nuclear factors to the 5'-flanking region of pituitary and placental members of the human growth hormone gene family.

Placental chorionic somatomammotropin (hCS-A or B) and growth hormone variant (hGH-V) are members of the human growth hormone family, and are related by structure and function to pituitary growth hormone (hGH-N). However, while the hGH-N gene is expressed specifically in the anterior pituitary, hGH-V and hCS are produced in the placenta. Hybrid hGH-N, hGH-V and hCS-A genes containing 5'-flanking sequences, including the endogenous promoter, are preferentially expressed in rat pituitary tumor (GC) cells, after gene transfer. Since interaction with a pituitary-specific protein (Pit 1) is required for efficient hGH-N as well as rat growth hormone (rGH) gene expression in GC cells, binding of pituitary proteins to the hGH-V and hCS-A promoter sequences was investigated. Rat Pit 1 binds at two locations on the hGH-N gene, a distal (-140/-107) and proximal site (-97/-66), in a similar manner to that observed with the rGH gene. By contrast, efficient Pit 1 binding was seen only to the distal site of the hGH-V gene and the proximal site of the hCS-A gene. Although binding of a protein to the distal hCS-A sequences was observed, the site of interaction was truncated (-140/-116), not pituitary-specific, and was more consistent with the binding of Sp1. These data indicate that rat Pit 1 binds to the placental hGH-V and hCS-A genes and correlates with their promoter activity in GC cells after gene transfer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Species-specific placental corticotropin releasing hormone messenger RNA and peptide expression.

The human placenta is a major site of synthesis of the hypothalamic neuropeptide corticotropin releasing hormone (CRH). We have examined placentae of several other species for expression of the CRH gene in this tissue. CRH mRNA was detected in human, gorilla, and rhesus monkey placentae, but not in rat, guinea pig and lemur placentae. A nonhuman primate may therefore be a suitable experimental model for studying placental CRH gene expression in vivo.

Animals↗
PubMed1997

Maternal growth hormone treatment increases placental diffusion capacity but not fetal or placental growth in sheep.

We tested the hypothesis that chronic maternal GH administration would increase fetal substrate supply, increase maternal and fetal insulin-like growth factor I (IGF-I) concentrations, and therefore enhance growth in the late gestation fetal sheep. Eleven ewes received bovine GH 0.1 mg/kg twice daily for 10 days, whereas 10 control ewes received saline. GH treatment increased placental capacity for simple diffusion (P < 0.01), with a trend toward an increase in placental capacity for facilitated diffusion (P = 0.07). GH treatment also lowered maternal and fetal blood urea concentrations, and there was a trend toward increased fetal protein oxidation (P = 0.07). Maternal but not fetal IGF-I and insulin concentrations increased. Fetal and placental growth were not altered by GH treatment. Maternal and fetal metabolic status was significantly affected by maternal food intake. We conclude that maternal GH treatment increases placental transport capacity, but that anabolic effects in the mother may limit fetal substrate supply and therefore prevent an increase in fetal growth.

Animals↗