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At least 1,027 records · Page 57Linked to original sources
PubMed2006

Corticotropin-releasing hormone inhibits progesterone production in cultured human placental trophoblasts.

Placental-derived corticotropin-releasing hormone (CRH) seems to play a major role in the mechanisms controlling human pregnancy and parturition. It has been suggested that CRH directly modulates the endocrine function of placental trophoblasts, including the production of estrogen, ACTH, and prostaglandin. In this study, we sought to investigate the effect of CRH, locally produced by placenta, on progesterone production. Percoll-purified placental trophoblasts were obtained from uncomplicated term pregnancies and cultured for 72 h. Progesterone concentration in culture media was measured by RIA. The mRNA transcripts encoding CYP11A1 and HSD3B1, the enzymes for progesterone synthesis, were determined by quantitative real-time reverse transcription (RT)-PCR. Results showed that CRH (10(-8)-10(-6) mol/l) caused a significant decrease in progesterone levels in a dose-dependent manner. The CRH antagonist, alpha-helical CRH 9-41, at 10(-7)-10(-5) mol/l stimulated progesterone secretion. Consistent with this thesis, CRH decreased, whereas alpha-helical CRH increased, the mRNA levels of CYP11A1 and HSD3B1. Since CRH has been shown to activate the phospholipase C-protein kinase C (PKC) signal pathway in placenta, we examined whether the effect of CRH on progesterone synthesis was dependent on PKC signal pathway. Treatment of cells with PKC inhibitor, Gö6976, resulted in a significant increase in progesterone production, and exogenous CRH restored progesterone production. In conclusion, placental CRH exhibits a tonic inhibitory effect on progesterone production in a PKC-dependent fashion.

Carbazoles↗
PubMed2006

Corticotropin-releasing hormone stimulates estrogen biosynthesis in cultured human placental trophoblasts.

Estrogens and corticotrophin-releasing hormone (CRH) produced by the placenta play pivotal roles in the control of parturition in human and other primates. There is a strong correlation between maternal CRH and estrogen concentrations throughout gestation. To investigate whether CRH produced locally in the placenta could modulate estrogen production, we obtained human placental trophoblasts from uncomplicated term pregnancies and cultured them for 72 h. Cells were then treated with CRH and with a CRH receptor antagonist, alpha-helical CRH9-41. The results showed that CRH stimulated, but alpha-helical CRH9-41 inhibited, the production of estradiol in a time- and dose-dependent manner. Consistent with this thesis, CRH increased whereas alpha-helical CRH decreased the mRNA levels of STS, CYP19A1, and HSD17B1, the key enzymes for estrogen synthesis. These results suggest that, in the placenta, endogenously produced CRH exhibits a tonic stimulatory effect on estrogen production.

Aromatase↗
PubMed1993

Adipsin expression and growth in rats as influenced by insulin and somatotropin.

Adipsin is a molecular marker of obesity in rodents. Content of adipsin protein in blood and mRNA in adipocytes is significantly reduced in several genetic and experimentally induced obese models. It has been suggested that this reduction in adipsin is causative to obesity development. Insulin reduces adipsin expression in vitro and is negatively correlated with adipsin expression in vivo. Because bovine somatotropin (bST) opposes many actions of insulin and can reduce body fat content, we tested the hypothesis that bST enhances adipsin expression. In two experiments using 210 rats, bST and a similar hormone, bovine placental lactogen (bPL), both caused a small (14 to 27%) but statistically significant reduction in circulating adipsin protein. Because exogenous bST can increase circulating insulin we next used a diabetic model to test the bST effect on adipsin. In rats treated with streptozotocin and injected daily with insulin (STZ+I), bST had no effect on circulating adipsin. Additional variables related to growth were influenced differently by bST in normal vs. STZ+I animals. In conclusion, the drop in circulating adipsin following bST administration in normal rats is dependent upon the animals' ability to secrete insulin.

Adipose Tissue↗
PubMed1988

Cloning and nucleotide sequence of placental hGH-V cDNA.

We have previously demonstrated the presence in human placenta and maternal serum of a GH variant, called human placental growth hormone (hPGH). We have also shown that the hGH-V gene is expressed at the placental level thus possibly coding for hPGH. The hGH-V cDNA has now been isolated from a lambda gt 11 human placenta cDNA library. Its sequence has been determined which firmly establishes the GH-V gene mode of splicing as well as the GH-V protein structure. Our data give final evidence of placental hGH-V gene expression and reinforce the hypothesis of identity between the hGH-V protein and hPGH.

Amino Acid Sequence↗
PubMed2002

Characteristics of the fetal/maternal interface with potential usefulness in the development of future immunological and pharmacological strategies.

A study of the fundamental biology of the maternal-fetal interface reveals the complex interactions among multiple cell types and regulatory factors necessary to support a successful pregnancy. Cells of decidua and trophoblast lineages play central roles in creating the maternal-fetal interface and are sources of regulatory factors that can determine the quality and success of pregnancy. The regulatory factors considered here are major placental histocompatibility complex proteins, pregnancy-specific regulatory factors for uterine inflammatory cells, and hormone-controlled placental multidrug-resistant transport systems. Potential targets are discussed and presented as areas where researchers may identify novel pharmacological and immunological strategies that eventually will extend to the clinic to improve the quality and success of pregnancy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1976

Synthesis of human placental lactogen in Xenopus oocytes.

Oocytes from Xenopus laevis were injected with polysomes from normal human term placenta. Synthesis of the protein hormone Human Placental Lactogen (HPL) in the oocytes was demonstrated by specific immunoprecipitation with anti-HPL serum. Analysis of the immunoprecipitates on SDS-polyacrylamide gel revealed one peak, with a migration distance corresponding exactly to that of [14C]-Radioacetylated HPL added as a marker. Two days after injection the mRNA was still able to direct the synthesis of HPL.

Animals↗
PubMed1999

A novel megakaryocyte differentiation factor from mouse placenta.

Megakaryocyte differentiation and subsequent platelet production are regulated by a network of growth factors and cytokines. We hypothesized that pregnancy-specific regulatory factors also may participate in the modulation of megakaryocytopoiesis and thrombopoiesis. We identified a mouse placental prolactin-like protein hormone with an activity similar to interleukin 6 in targeting megakaryocytes and inducing cell differentiation. The receptor for this placental hormone is present on megakaryocytes from pregnant and nonpregnant female mice and from male mice, and from humans, suggesting that this signaling pathway (if not necessarily this particular ligand) is broadly functional both in terms of physiologic state and evolution. Thus, studying the biologic activities of the large family of placental prolactin-like proteins represents a potentially valuable approach to the discovery of novel hematopoietic signaling pathways.

Animals↗
PubMed1994

Mouse placental cells secrete immunoreactive growth hormone-releasing factor.

The initial objective of this study was to establish a placental cell culture system in which the secretion of mouse growth hormone-releasing factor (mGHRF) could be examined during a several-day period. To determine when during pregnancy placental cells begin to express mGHRF, Northern blot analysis was carried out on total RNA from placentas collected on Days 6, 9, 11, 13, 15, 17, and 18 of pregnancy. Mouse GHRF mRNA could be detected as early as Day 11 of pregnancy. Its steady-state levels increased to maximum values on Days 15-17 and then declined slightly on Day 18. Placentas from Day 12 of pregnancy were selected for cell culture. The basal zone and labyrinth were dispersed in collagenase, and the cells were fractionated on a Percoll gradient. Two bands of cells were selected for further study. Both released significant amounts of immunoreactive mGHRF during a 5-day culture period. Effects of prolonged exposure of the cells to 8-bromo-cAMP and to agents that elevate intracellular cAMP concentration were then examined. Treatment of the cells with 0.5 mM 8-bromo-cAMP resulted in a significant decrease in the mGHRF concentration of the medium by the second day of culture. Mouse GHRF secretion was also inhibited by treatment of the cells with 100 ng/ml cholera toxin or 0.1 mM forskolin. The effect of 8-bromo-cAMP was concentration-dependent, with 0.1 mM being the lowest concentration that was active. 8-Bromo-cAMP treatment also reduced the steady-state level of mGHRF mRNA in the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗