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Results for “PLACENTAL HORMONES”

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At least 73 records · Page 4Linked to original sources
PubMed1995

[Impact of placental hormone withdrawal on postpartum depression].

Prenatal and postpartum measurements of serum beta-hCG, estradiol (E2) and progesterone (P) concentration were done by radioimmunoassay in 20 cases of postpartum depression (PD) and 20 cases without postpartum depression (NPD). The results showed significantly higher serum levels of P and beta-hCG (at 36-37 gestational week) in PD, but no difference in the serum P and beta-hCG concentration between the PD and NPD after childbirth. The falling of the two hormones was faster in PD than in NPD. In neither prenatal nor postpartum test was any difference seen in serum E2 concentration between PD and NPD. These results suggest that supposely, the endogenous risk factor, the rapid withdrawal of the placental hormones (P and beta-hCG) after delivery, leads to PD.

Chorionic Gonadotropin↗
PubMedDate not supplied

Placental hormones: I. Immunofluorescence studies of the localization of chorionic gonadotrophin, placental lactogen and prolactin in human and rat placenta and in the endometrium of pregnant rats.

Chorionic gonadotrophin (CG), placental lactogen (PL) and prolactin (PRL) were localized in sections of human and rat placenta using the indirect immunofluorescence technique. Antisera were absorbed with homologous and unrelated antigens by affinity chromatography or complexed with their respective antigens. To exclude binding of IgG and immune complexes to Fc-receptor in chorionic tissue, thus leading to erroneous results, sections were preincubated with an excess of rat IgG. The results indicate that, in the human placenta, human CG (hCG) and human PL (hPL) can be identified in the syncytiotrophoblast. Using antibodies to hPRL fluorescence was found in giant cells within the cytotrophoblastic islands in the intervillous space and in cytotrophoblastic cells within placental septa. In the rat placenta rat PL (rPL) and rat PRL (rPRL) could be identified in the giant cells of the basal zone. Furthermore rPRL/rPL was localized in the endometrium and adjacent decidial cells of rat pregnancy. No staining of chorionic cells was detected using antibodies against hCG and bLH, which cross-reacted with rLH. These experiments provide further evidence that the rat placenta is unlikely to produce a CG/LH-like hormone.

Animals↗
PubMed1991

Retinoic acid stimulates placental hormone secretion by choriocarcinoma cell lines in vitro.

Retinoic acid (RA), an active metabolite of vitamin A, is an important mediator of cellular differentiation and has been shown to stimulate human CG (hCG) secretion by JEG-3 choriocarcinoma cells in vitro. In order to determine whether RA stimulates the hCG secretion by other trophoblastic cell lines, we evaluated the effect of RA on hCG, hCG-alpha subunit (hCG-alpha), and progesterone secretion in three choriocarcinoma cell lines: JEG-3, JAR, and BeWo. RA stimulated hCG and hCG-alpha secretion in a dose-dependent fashion by each of the three cell lines. The time required to give a statistically significant increment of hCG and hCG-alpha over control cells was 48 h. The addition RA to cholera toxin (10 micrograms/ml) resulted in an additive or synergistic stimulation of hCG and hCG-alpha secretion by the three cell lines. Cycloheximide (1 microM) abolished the effect of RA on hCG and hCG-alpha secretion in the BeWo cell line. Progesterone secretion in response to RA was inconsistent. Progesterone secretion by both JEG-3 and BeWo cell lines were stimulated at high concentrations of RA (1 x 10(-6], whereas progesterone secretion by JAR cells was not stimulated. Intracellular levels of cAMP were not affected by RA treatment in the JEG and JAR cells. In the dosages used, RA did not significantly alter cell number in any of the cell lines. RA in physiologic concentrations stimulates hCG and hCG-alpha secretion by three choriocarcinoma cell lines in vitro. Whether RA is a physiologic mediator of placental hormone production is unknown.

Cell Line↗
PubMed1975

A human placental hormone (UTPH) with uterine growth and DNA promoting effects.

A human placental protein previously described is studied in order to expand its biological characterization. Dose-response-curve of its action on uterine growth of prepuberal mice showed to be a significant logarithmic function and this effect is neutralized by its specific antiserum. It is also demonstrated that the uterine growth-promoting effect is not due either to estrogen, protein-bound estrogen, progesterone or chorionic gonadotrophin. Experimental evidence is given to demonstrate that the mechanism of action of this placental protein is to stimulate the synthesis and to increase the concentration of DNA in uterine tissue, differing then in this respect from the effect of estrogen. Previous work has shown that this placental protein is present in full-term placentas within similar ranges as HCG and HPL. It is also detected in blood during pregnancy and acts biologically in at least two target organs: uterus and mammary gland. Therefore the name of uterotrophic placental protein (UTPH) has been suggested for this substance.

Animals↗
PubMed2000

Inhibition of tumor growth by the antiangiogenic placental hormone, proliferin-related protein.

Proliferin-related protein (PRP) is a potent placental antiangiogenic hormone. To test the antiangiogenic potential of PRP to block tumor growth, we engineered tumor cells to express this hormone. Both SV40-transformed BALB/c mouse 3T3 fibroblasts and rat C6 glioma cells have markedly reduced growth rates as tumors in mice if they express high levels of PRP. In both models, the small tumors that form are largely avascular, whereas control tumors are rich in blood vessels, consistent with PRP limiting tumor growth by preventing neovascularization of the tumors. The antiangiogenic effects of PRP are also detected on human endothelial cells, suggesting that the receptor and signaling pathway of this mouse hormone are conserved between mouse and human and may represent useful targets for the development of antiangiogenic therapeutics. That signaling pathway appears to involve an inhibition of arachidonic acid release, based on the ability of arachidonic acid to overcome the antiangiogenic effects of PRP.

3T3 Cells↗
PubMed1996

[The testis as eutopic production site of human growth hormone, placental lactogen and prolactin: possible autocrine/paracrine effects on testicular function].

The human (h) protein hormones, growth hormone (hGH-N) and prolactin (hPRL), are mainly produced in the pituitary, whereas the human placenta expresses the other four members of the protein hormone gene family, designated placental lactogens (PL-A, PL-B, PL-L) and growth hormone variant (GH-V), GH-N stimulates somatic growth, supports nitrogen-, phosphate- and potassium retention and promotes lipolytic and anabolic metabolism, whereas PRL acts on the mammary gland and induces mammogenesis, lactogenesis and galactopoesis. Both hyperprolactinemia and growth hormone deficiency affect the onset of puberty and reproduction in man and mice. In addition to the glycoprotein hormones, these hormones play a role in the maintenance of testicular function. Our group previously demonstrated eutopic production of glycoprotein hormones hLH (human luteinizing hormone) and hCG (human chorionic gonadotropin) in the testis. We have now extended our investigations to the local testicular expression of protein hormones. By means of the molecular biology techniques of the reverse transcription-polymerase chain reaction (RT-PCR), Southern blot and by restriction endonuclease analyses of the generated PCR products we demonstrated the eutopic expression of genes coding for the protein hormones. GH-N gene transcripts were detected only in the pituitary and abundant PL-A/B and a few GH-V gene transcripts were demonstrable in the placenta. In contrast, in the testis GH/PL and PRL genes are transcribed. Since testicular protein hormone gene expression is rather low, these hormones may act locally and not as systemic factors; they presumably modulate the LH/CG-mediated testosterone biosynthesis and/or may act on the spermatogenesis.

Animals↗