Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLACENTAL EXTRACTS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources
PubMed1977

Absence of placental transfer of l-triiodothyronine (T3) in the rat.

To detect placental transfer of L-triiodothyronine (T3) in pregnant rats, we injected 1 muCi [125I]T3 on the 16th, 18th, and 20th day of gestation. Three hours after the injection, which corresponds to the equilibrium time determined by a method of constant infusion, the pregnant rats and their fetuses were killed. The [125I]T3 was extracted from the serum or the homogenate by butanol extractions and alkaline washes. The transfer rate was calculated from the quantity of [125I]T3 in the serum of the fetuses after 3 hr and from the maternal metabolic clearance rate (8.19 +/- 0.45 ml/hr/100 g body weight; mean +/- SEM). At the 16th day of gestation, the placental transfer of T3 was 0.82 +/- 0.11% of the total maternal clearance rate/litter weight; it was 1.05 +/- 0.25% at the 18th day of gestation and 0.58 +/- 0.10% at the 20th day of gestation. There were no significant differences between these results. The maternal T3 concentration was 68.27 +/- 20.6 ng/100 ml and its production rate was 5.57 +/- 0.31 ng/hr/100 g; with these data we calculated a maternal-fetal T3 transfer of 46 +/- 6 pg/hr. Furthermore, there was no T3 transfer observed when the mother received 1.9 mug unlabeled T3, which led to a significant rise in maternal T3 concentration (68.27 +/- 20.6 ng to 102.23 +/- 7.41 ng/100 ml; P less than 0.01); there was no detectable T3 in the fetal serum. From these results we conclude that there is minimal or no placental transfer of T3 in the rat and that the hypothalamic-pituitary-thyroid axis of the fetus develops autonomously.

Animals↗
PubMed1995

Angiogenesis and the placental environment.

Rapid growth and vascularization of the human placenta are characteristic of early pregnancy and are accomplished in an unusually hypoxic environment. Stimulation of placental growth through hypoxia-induced angiogenesis may therefore be of particular importance. We have previously found that several varieties of vascular endothelial growth factor (VEGF) mRNA, including VEGF165, are present in cultured placental fibroblasts. We hypothesized that hypoxia would increase the transcription and translation of VEGF by these cells and provide one mechanism linking placental development with its environment. Placental fibroblasts were grown in aerobic or anaerobic atmospheric conditions for 72 h. By 24 h the oxygen tension of the anaerobic culture media was significantly less than that of the aerobic cultures. RNA was extracted from the cells at 24, 48 and 72 h. Following reverse transcription polymerase chain reaction (RT-PCR) stronger signals for VEGF were always found in the anaerobic cultures and this was confirmed by competitive PCR. mRNA for VEGF165 was represented most strongly but the anaerobic cultures also showed clearly mRNA for VEGF121, VEGF189 and VEGF206. The VEGF protein was also measured in the aerobic and anaerobic culture medium. By 72 h the average concentration of VEGF was significantly higher (P = 0.01) in the anaerobic culture medium. VEGF production is one mechanism through which oxygen supply may influence placental development. Examples of this may include the compensatory placental hypertrophy associated with maternal anaemia and with reproduction at high altitude.

Alternative Splicing↗
PubMed2006

Egr-1 transcription activation exists in placental endothelium when vascular disease is present.

OBJECTIVE: To seek evidence of early vascular injury in the placental villous microcirculation in placental insufficiency identified by a high-resistance umbilical Doppler study by examining for expression of fibroblast growth factor receptor-1 (FGFR-1), its transcription factor, early growth response factor-1 (Egr-1) and plasma fibroblast growth factor-2 (FGF-2). DESIGN: Case-control study. SETTING: University teaching hospital. SAMPLE: Placentas and umbilical vein blood were collected at delivery from 12 women with normal pregnancy delivered at term and 14 with placental vascular disease defined by an abnormal umbilical artery Doppler study. METHODS: Microvascular endothelial cells were isolated from fresh human placentas using collagenase digestion and Dynabeads coated with monoclonal antibody against CD31. RNA was extracted from the isolated endothelial cells. The messenger RNA (mRNA) expression of FGFR-1 and Egr-1 production were assessed by reverse transcription polymerase chain reaction and factored relative to 18S ribosomal RNA. To confirm that FGF-2 was playing a significant role in this microvascular endothelial cell injury in the placenta, we also measured the soluble fraction of FGF-2 in fetal plasma from same groups of pregnancies using an enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Microvascular endothelial cells expression of Egr-1mRNA, FGFR-1 mRNA and presence of soluble FGF-2 in fetal plasma. RESULTS: The soluble level of FGF-2 in the fetal placental circulation from pregnancy with placental vascular disease was increased when compared with normal pregnancy (median 10.15 pg/ml and interquartile range 5.34-21.83 pg/ml versus 4.46 pg/ml and 3.69-5.66 pg/ml; P < 0.05). Microvascular endothelial cells from the placental villi with placental vascular disease showed upregulation of both FGFR-1 mRNA expression (median 0.72 and interquartile range 0.40-1.64 versus 0.34 and 0.19-0.71; P<0.05) and Egr-1 expression (median 0.79 and interquartile range 0.27-1.86 versus 0.23 and 0.17-0.67; P<0.05) in comparison with normal pregnancy. CONCLUSIONS: Endothelial cells from the placental villi are upregulated for expression of Egr-1 transcription factor gene in placental vascular disease. The FGFR-1 activation and increase in FGF-2 in the fetal circulation are known to be very early features of the response of endothelium to injury. Egr-1 is a promoter of many key pathophysiologically relevant target genes, which influence the development of subsequent vascular lesions. This change may occur before the pathological features recognised on microscopy.

Case-Control Studies↗
PubMed1987

Metabolic quotients and oxygen extraction across the uterus of the post-term pregnant rabbit under chronic steady-state conditions.

The extraction of oxygen by the uterus in the term rabbit has been found to be very high. During post-term pregnancy, the fetuses of the rabbit are approximately 40% larger, despite a reduction in placental weight of approximately 30%. The purpose of our study was to investigate the changes that occur in the maternal rabbit to allow survival of the fetus under these conditions. Post-term pregnancies were induced in 5 white New Zealand rabbits by injections of chorionic gonadotropin and progesterone on the 26th day of gestation. Catheters were placed surgically on day 28, and blood samples were taken daily from the femoral artery and uterine veins starting at day 31. Each sample was analyzed for pH, PCO2, PO2, oxygen capacity and saturation, glucose, beta-hydroxybutyrate, lactate and acetoacetate. Coefficients of extraction were calculated for oxygen and metabolic quotients were calculated for each substrate. These data are compared with those obtained for the term rabbit in previous studies. There was a significant increase in the coefficient of oxygen extraction in the post-term animals; however, the metabolic quotients across the uterus were not significantly different between the term and the post-term rabbit.

Animals↗
PubMed1997

Coordinate expression of inducible nitric oxide synthase and cyclooxygenase-2 genes in uterine tissues of endotoxin-treated pregnant mice.

OBJECTIVES: Our purpose was to investigate the relationship between expression of cyclooxygenase-2 and inducible nitric oxide synthase genes after labor induction with bacterial lipopolysaccharide in a murine model of preterm parturition. STUDY DESIGN: Pregnant C57B1/6 mice were given Escherichia coli lipopolysaccharide (20 micrograms per mouse) by intraperitoneal injection on day 16 of gestation, and the animals were followed up for signs of labor. Control mice received an equivalent volume of 0.9% saline solution. The latency from lipopolysaccharide injections until appearance of the first pup was recorded. Two separate groups of mice were given either aminoguanidine or indomethacin (5 mg/kg intragastric) 24 hours before induction of preterm labor. In a separate set of experiments mice were treated with lipopolysaccharide as described and were killed at intervals from 0.5 to 72 hours and intrauterine tissues (uterus, placenta, and fetal membranes) were removed and snap frozen in liquid nitrogen. Total protein and ribonucleic acid were extracted for Western and Northern blot analysis of cyclooxygenase-2 and inducible nitric oxide synthase protein and messenger ribonucleic acid, respectively. RESULTS: Northern blots from uterine, placental, and fetal membrane tissues of lipopolysaccharide- and saline solution-treated mice revealed that cyclooxygenase-2 and inducible nitric oxide synthase messenger ribonucleic acid transcripts were rapidly (within 0.5 to 2 hours) up-regulated after lipopolysaccharide administration but were unchanged in mice injected with saline solution. Immunoblot analysis with isoform-specific antibodies revealed that both enzymes were expressed in uterus, placenta, and fetal membranes in a coordinated fashion with peak expression seen at 6 to 8 hours. Although the steady-state accumulation of messenger ribonucleic acid transcripts encoding cyclooxygenase-2 and inducible nitric oxide synthase peaked at 6 hours and declined to baseline by 16 hours after injection with lipopolysaccharide, expression of cyclooxygenase-2 and inducible nitric oxide synthase was sustained through the period when premature delivery was observed. Nitric oxide-dependent cyclooxygenase-2 and inducible nitric oxide synthase expression was demonstrated by the elimination of accumulation of both messenger ribonucleic acid transcripts in mice pretreated with aminoguanidine before injection with lipopolysaccharide. CONCLUSIONS: These data indicate that nitric oxide synthesis may be a prerequisite for subsequent stimulation of cyclooxygenase-2 and inducible nitric oxide synthase gene expression. Taken together, the data suggest that cyclooxygenase-2 and inducible nitric oxide synthase are expressed in a coordinated manner in the uterus of endotoxin-challenged pregnant mice and that their enzymatic products may contribute to the signaling of uterine activity or cervical changes culminating in expulsion of the fetus.

Animals↗
PubMedDate not supplied

Extracellular binding of calcium in the guinea-pig placenta.

Extraction of 45Ca from the perfused umbilical vascular bed of the guinea-pig placenta was measured using 3H-sucrose or 24Na as reference substances at a constant inflow concentration of the tracers. La3+ (5mM) depressed extraction of 45Ca below zero for several minutes. This suggests that there is a significant amount of Ca bound extracellularly on the umbilical side of the placental barrier.

Animals↗
PubMed2000

Inositol phosphoglycans and signal transduction systems in pregnancy in preeclampsia and diabetes: evidence for a significant regulatory role in preeclampsia at placental and systemic levels.

Measurements have been made of the urinary content of inositol phosphoglycans IPG P-type and IPG A-type, putative insulin second messengers, in preeclampsia, in type I insulin-treated diabetic pregnant women and their matched control subjects, and nonpregnant women of child-bearing age. The content of IPG P-type and IPG A-type was also measured in the placenta from preeclamptic patients and from normal pregnancies. Pregnancy was associated with an increase, approximately twofold, in urinary output of IPG-P-type relative to nonpregnant controls (P<0.01). The 24-h output of IPG P-type in urine in preeclamptic women was significantly higher (2- to 3-fold) than in pregnant control subjects matched for age, parity, and stage of gestation (P<0.02). In contrast, insulin-dependent diabetic pregnant women did not show any significant change in urinary output of IPG P-type or IPG A-type relative to pregnant control subjects. Evidence for a possible relationship and correlation between the urinary excretion of IPG P-type and markers of preeclampsia, including proteinuria (r = 0.720, P<0.01), plasma aspartate transaminase (r = 0.658, P<0.05), and platelet counts (r = 0.613, P<0.05) is presented. A high yield of IPG P-type was extracted from human placenta, in preeclampsia some 3-fold higher (P = 0.03) than the normal value, whereas no IPG A-type (with lipogenic-stimulating activity) was found. Low concentrations of placental IPG A-type were detected relative to IPG P-type using assay systems dependent upon the effect of this mediator on cAMP-dependent protein kinase or on a proliferation assay using thymidine incorporation into DNA of EGFR T17 fibroblasts. It is postulated that the high urinary excretion IPG P-type in preeclampsia reflects high placental levels and relates to the accumulation of glycogen in the placenta. The paracrine effects of placental IPG P-type (stimulation off other endocrine glands and/or endothelial cells) could contribute to the pathogenesis of the maternal syndrome. A possible theoretical link between elevated placental IPG P-type and apoptosis is proposed.

Adult↗
PubMed1990

Multiple adenosine 3',5'-cyclic [corrected] monophosphate response element DNA-binding proteins generated by gene diversification and alternative exon splicing.

The protein sequence deduced from the open reading frame of a human placental cDNA encoding a cAMP-responsive enhancer (CRE)-binding protein (CREB-327) has structural features characteristic of several other transcriptional transactivator proteins including jun, fos, C/EBP, myc, and CRE-BP1. Results of Southwestern analysis of nuclear extracts from several different cell lines show that there are multiple CRE-binding proteins, which vary in size in cell lines derived from different tissues and animal species. To examine the molecular diversity of CREB-327 and related proteins at the nucleic acid level, we used labeled cDNAs from human placenta that encode two different CRE-binding proteins (CREB-327 and CRE-BP1) to probe Northern and Southern blots. Both probes hybridized to multiple fragments on Southern blots of genomic DNA from various species. Alternatively, when a human placental c-jun probe was hybridized to the same blot, a single fragment was detected in most cases, consistent with the intronless nature of the human c-jun gene. The CREB-327 probe hybridized to multiple mRNAs, derived from human placenta, ranging in size from 2-9 kilobases. In contrast, the CRE-BP1 probe identified a single 4-kilobase mRNA. Sequence analyses of several overlapping human genomic cosmid clones containing CREB-327 sequences in conjunction with polymerase chain reaction indicates that the CREB-327/341 cDNAs are composed of at least eight or nine exons, and analyses of human placental cDNAs provide direct evidence for at least one alternatively spliced exon. Analyses of mouse/hamster-human hybridoma DNAs by Southern blotting and polymerase chain reaction localizes the CREB-327/341 gene to human chromosome 2. The results indicate that there is a dichotomy of CREB-like proteins, those that are related by overall structure and DNA-binding specificity as well as those that are related by close similarities of primary sequences.

Amino Acid Sequence↗
PubMed1986

The effects of hypoxanthine on methotrexate-induced differentiation of cultured human choriocarcinoma (BeWo) cells.

When cultured human choriocarcinoma (BeWo) cells are exposed to methotrexate, proliferation ceases and cells undergo a complex differentiative response that resembles development of normal trophoblast. Although thymidylate starvation has been shown to be causative in methotrexate-induced expression of syncytiotrophoblastic markers by BeWo cells, the role of purine deprivation is uncertain since previous studies utilized growth media containing exogenous purines. This work investigated the effects of hypoxanthine on methotrexate-induced cell enlargement, expression of placental alkaline phosphatase, and morphological differentiation to the syncytiotrophoblast-like phenotype. When methotrexate exposures (1 microM, 48 h) were conducted in a purine-free basal medium supplemented with dialyzed fetal bovine serum, RNA synthesis was greatly reduced and cell enlargement did not occur. Specific methods for removing purines (charcoal extraction and xanthine oxidase treatment) decreased the ability of serum to support cell enlargement during methotrexate exposures, whereas addition of hypoxanthine to culture fluids restored its ability to support maximal increases in cell mass, confirming that purines were the factors lost during dialysis. In contrast, morphologically differentiation to the syncytiotrophoblast-like phenotype and increased expression of placental alkaline phosphatase were unaffected by the availability of purines during exposure to methotrexate.

Alkaline Phosphatase↗
PubMedDate not supplied

Apparent role of the macrophage growth factor, CSF-1, in placental development.

Colony stimulating factor-1 (CSF-1) is a glycoprotein growth factor required for the proliferation and differentiation of mononuclear phagocytic cells (reviewed in ref. 1). A 10,000-fold elevation of mouse uterine CSF-1 during pregnancy, suggested by studies of the bone marrow colony stimulating activity of uterine extracts, was recently demonstrated by radioimmunoassay (RIA). This increase and the observations that placenta and choriocarcinoma cell lines express c-fms messenger RNA and the c-fms proto oncogene product (CSF-1 receptor) respectively, suggest an additional role for CSF-1 in pregnancy. We now show that uterine CSF-1 concentration is regulated by the synergistic action of female sex steroids, oestradiol-17 beta (E2) and progesterone (P) and that the elevation in CSF-1 concentration can be attributed to the preferential expression of an alternatively spliced CSF-1 mRNA by uterine glandular epithelial cells. These findings indicate that CSF-1, under hormonal influence, plays a role in placental development and function and that steroid hormones may regulate developmental processes via their effects on the expression of tissue-specific growth factors.

Animals↗
PubMedDate not supplied

Determination of didanosine in maternal plasma, amniotic fluid, fetal and placental tissues by high-performance liquid chromatography-tandem mass spectrometry.

A rapid and efficient high-performance liquid chromatography (HPLC)-tandem mass spectrometry method for the determination of didanosine concentrations in maternal rat plasma, amniotic fluid, placental and fetal tissue samples has been developed and validated. Tissue samples were homogenized in optima water and centrifuged. The supernatant was subjected to solid-phase extraction (SPE) prior to analysis. Plasma and amniotic fluid samples were extracted without pretreatment. An Agilent 1100 Series HPLC coupled with a Micromass Quattro II triple quadrupole mass spectrometer was used for all analyses. Chromatographic resolution was achieved on a Nova-Pak phenyl analytical column (2.0 x 150 mm, 4 microm particle size) equipped with a Phenomenex Security-guard phenyl guard cartridge (2.0 x 4.0 mm) using 60% methanol in 10 mm ammonium acetate buffer mobile phase for all matrices at a flow rate of 0.15 mL/min. The method yields retention times of 2.9 min for didanosine and 3.0 min for the internal standard, stavudine. Limits of detection were 1 ng/mL for all matrices. Recoveries were 70% or greater for both compounds in the different matrices. Within- and between-run precision (%RSD) and accuracy (%error) was less than 15% for all matrices.

Amniotic Fluid↗
PubMed1975

Enzymes of normal and malignant trophoblast: phosphoglucose isomerase, phosphoglucomutase, hexokinase, lactate dehydrogenase, and alkaline phosphatase.

In this study we compare the specific activities and isoenzyme patterns of five enzymes--phosphoglucose isomerase, phosphoglucomutase, hexokinase, lactate dehydrogenase, and alkaline phosphatase--in term placenta with the analogous enzymes in a clone of choriocarcinoma cells grown in culture. Phosphoglucose isomerase, phosphoglucomutase, and lactate dehydrogenase specific activities of the choriocarcinoma did not differ by more than two or three times from the mean activities of the comparable enzymes in placenta; the specific activity of hexokinase in the choriocarcinoma amounted to 14 per cent of the mean value for placenta. In contrast, the mean specific activity of heat-stable alkaline phosphatase in the choriocarcinoma amounted to only 1 per cent of the mean value for placenta. By growing the cells in 5-bromodeoxyuridine, 20 mug per milliliter, we were able to increase alkaline phosphatase activity to 68 per cent of the mean value for placenta. For both extracts, phosphoglucose isomerase zymograms were similar and phosphoglucomutase zymograms were similar. The hexokinase zymogram of term placenta showed two isoenzymes which stained more intensely with 0.5 mM. glucose than with 0.1M glucose. A hexokinase isoenzyme was observed in zymograms of both extracts which stained more intensely with 0.1M glucose than with 0.5 mM glucose. Lactate dehydrogenase exhibited an extra isoenzyme in the choriocarcinoma extract. When the cells were cultivated in medium containing 5 mug per milliliter of 5-bromodeoxyuridine, the induced phosphatase in the cell line was electrophoretically similar to placental phosphatase. At higher concentrations of 5-bromodeoxyuridine, the most anodal isoenzyme was 0.5 cm. slower in mobility than the comparable placental isoenzyme.

Alkaline Phosphatase↗
PubMed1999

Obstetric complications and the risk of schizophrenia: a longitudinal study of a national birth cohort.

BACKGROUND: Numerous epidemiological studies found an increased risk of schizophrenia among persons exposed to various obstetric complications. The underlying mechanisms are unknown. OBJECTIVE: To study specific risk factors, as well as sets of risk factors, representing 3 different etiologic mechanisms: (1) malnutrition during fetal life; (2) extreme prematurity; and (3) hypoxia or ischemia. METHODS: In this longitudinal cohort study, information in the National Birth Register was linked to the National Inpatient Register. We followed up 507516 children born between 1973 and 1977 with regard to a diagnosis of schizophrenia between 1987 and 1995 (238 cases). By record linkage, we also had access to data on psychiatric illness in the mother. Occurrence of schizophrenia was measured by the Mantel-Haenszel test and logistic regression. RESULTS: A number of specific risk factors were associated with an increased risk of schizophrenia. The relative risk (95% confidence interval) for preeclampsia was 2.5 (1.4-4.5); vacuum extraction, 1.7 (1.1-2.6); and malformations, 2.4 (1.2-5.1). In logistic regression models, we found that indicators of all 3 etiologic mechanisms were associated with increased point estimates of schizophrenia, although at lower risk levels. Preeclampsia, an indicator of fetal malnutrition, was the only risk factor with statistically significant increased risk after control for all potentially confounding factors. CONCLUSION: This study supports the theory of an association between obstetric complications and schizophrenia. Although preeclampsia was the strongest individual risk factor, there was evidence of increased risk associated with all 3 etiologic mechanisms.

Adult↗
PubMed1987

Adenosine 3',5'-monophosphate, prostaglandins, and epinephrine stimulate the secretion of immunoreactive gonadotropin-releasing hormone from cultured human placental cells.

Cell culture and biochemical procedures were used to identify and study the possible mechanisms regulating the secretion of GnRH-like immunoreactivity (GnRH-LI) from human placenta. Monolayer primary cultures of trophoblasts were established after mechanical and enzymatic dispersion of normal human term placenta. The cultured cells stained immunocytochemically positive with anti-GnRH serum, and GnRH-LI extracted from the cells eluted from high performance liquid chromatography with the same retention time as authentic GnRH. One week after plating, exposure to high concentrations of K+ or to various doses of veratridine, a Na+ ionophore, increased GnRH-LI release into the culture medium. This effect was reversed by Ca2+ antagonists (cobalt, EGTA, and verapamil). Dibutyrylcyclic AMP, forskolin, theophylline, and theobromine also increased GnRH-LI concentrations in the medium of cultured placental cells in a dose-related manner, as did prostaglandins E2 and F2 alpha and epinephrine. The effect of epinephrine on GnRH-LI concentrations was mimicked by isoproterenol and reversed by propranolol, suggesting an effect mediated by beta-adrenergic receptors. These results indicate that GnRH-LI release from cultured human placental cells is stimulated by the opening of ionic channels and activation of the adenylate cyclase/cAMP system, and that prostaglandins and epinephrine may be involved in the regulation of GnRH-LI release from human placenta.

Adenosine Monophosphate↗
PubMed2005

Chorionic mRNA expression and N-glycodiversity of pregnancy-associated glycoprotein family (PAG) of the European bison (Bison bonasus).

Placental PAG mRNA expression and N-glycodiversity of multiple PAG proteins secreted in vitro by trophectoderm (chorion epithelium) of wild pecoran Bovidae taxons was not examined previously. The study on European bison (Eb) aimed: (1) to determine placental PAG mRNA expression by in situ hybridisation; (2) to identify a profile of pecoran PAG protein family secreted in vitro by cotyledonary (CT) explants; (3) to examine N-glycodiversity of the PAG proteins in this wild taxon. In addition, we compared (4) a profile and N-glycodiversity of the PAG protein family secreted in vitro by CT and interCT-trophectoderm (intCT-TRD) explants of domestic ruminants. Cotyledonary sections of the Eb were used for in situ hybridisation (ISH) with (35)S-labelled probes produced with porcine PAG cDNA as templates. Various CT and intCT-TRD explants were long-term cultured in vitro. Chorionic proteins were isolated from media, ultra-filtrated (>10 kDa MWCO) and analysed by PAGE-Western blotting with various polyclonal anti-PAG sera. Protein samples with or without enzymatic deglycosylation were examined after different times of explant cultures. Released chorionic proteins were deglycosylated by N-glycanase F (PNGase F+) and compared to glycosylated forms (PNGase F-). This is the first paper demonstrating the PAG-like mRNA transcript expression (by ISH) and N-glycodiversity of immuno-reactive PAG-like proteins (produced in vitro by chorionic explants) of European bison. Various PAG proteins of Eb (EbPAG) were secreted by CT explants during long-term in vitro studies. Major approximately 78, approximately 67 and approximately 65 kDa EbPAG-like proteins were reduced by enzymatic deglycosylation (at least by 10 kDa). Considerably smaller amounts of approximately 45 kDa EbPAG-like proteins were also observed. In addition, we have found that various PAG proteins (30-73 kDa) were secreted by bovine CT explants, during long-term in vitro cultures. Corresponding amounts of PAG proteins, similar in M(r), were also secreted by intCT-TRD explants, whose tissues were not utilised for PAG protein extraction during other scientists' previous studies. It seems that the M(r)-heterogeneity and N-glycodiversity of the PAG protein family can play very important role during feto-placental interactions in Bovidae species.

Animals↗
PubMed1989

Plasma GHRH, CRH, ACTH, beta-endorphin, human placental lactogen, GH and cortisol concentrations at the third trimester of pregnancy.

UNLABELLED: The aim of the study was to determine the concentration of GHRH and CRH in maternal plasma during the 3rd trimester of pregnancy and to search for the possible correlations with related hormones such as ACTH, beta-endorphin, cortisol, GH and human placental lactogen. Patients consisted of 31 healthy pregnant women (20-39 years) divided according to duration of pregnancy into 2 groups: I. from 26 to 32 pregnancy week N = 13), II. from 33 to 39 week (N = 18), and of 7 women evaluated 3 days after delivery. All listed hormones except ACTH were measured by RIA (GHRH, CRH and beta-endorphin-like immunoreactivity after extraction with silic acid) and ACTH by IRMA. In the late 3rd trimester plasma levels of CRH (P less than 0.001), ACTH (P less than 0.02), beta-endorphin (P less than 0.05), cortisol (P less than 0.025), as well as GHRH (P less than 0.002) and human placental lactogen (hPL) (P less than 0.001) were increased in comparison to early 3rd trimester, whereas 3 days after delivery CRH and GHRH became undetectable and those of ACTH and cortisol decreased significantly. The CRH plasma concentrations were found to be strongly correlated with gestational age (r = 0.86, P less than 0.001) but not with ACTH and cortisol. GHRH levels correlated mainly with human placental lactogen concentrations (r = 0.64, P less than 0.001). CONCLUSION: In maternal plasma at the 3rd trimester of pregnancy, apart from the known markedly elevated CRH, the GHRH level was also raised. Strong correlations between CRH and gestational age and those between GHRH and human placental lactogen suggest that there is a relationship between these neurohormones and the placental function.

Adrenocorticotropic Hormone↗