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PubMed2000

The roles of placental growth hormone and placental lactogen in the regulation of human fetal growth and development.

The human growth hormone (hGH)/human placental lactogen (hPL) gene family, which consists of two GH and three PL genes, is important in the regulation of maternal and fetal metabolism and the growth and development of the fetus. During pregnancy, pituitary GH (hGH-N) expression in the mother is suppressed; and hGH-V, a GH variant expressed by the placenta, becomes the predominant GH in the mother. hPL, which is the product of the hPL-A and hPL-B genes, is secreted into both the maternal and fetal circulations after the sixth week of pregnancy. hGH-V and hPL act in concert in the mother to stimulate insulin-like growth factor (IGF) production and modulate intermediary metabolism, resulting in an increase in the availability of glucose and amino acids to the fetus. In the fetus, hPL acts via lactogenic receptors and possibly a unique PL receptor to modulate embryonic development, regulate intermediary metabolism and stimulate the production of IGFs, insulin, adrenocortical hormones and pulmonary surfactant. hGH-N, which is expressed by the fetal pituitary, has little or no physiological actions in the fetus until late in pregnancy due to the lack of functional GH receptors on fetal tissues. hGH-V, which is also a potent somatogenic hormone, is not released into the fetus. Taken together, studies of the hGH/hPL gene family during pregnancy reveal a complex interaction of the hormones with one another and with other growth factors. Additional investigations are necessary to clarify the relative roles of the family members in the regulation of fetal growth and development and the factors that modulate the expression of the genes.

Embryonic and Fetal Development↗
PubMed1979

[Interaction of placental hormones in mother-embryo system (author's transl)].

Described in this paper is the relationship between chorionic gonadotrophin, placental lactogen, progesterone, oestradiol and oestriol in the blood of mother and embryo. The concentrations of human chorionic gonadotrophin (HCG) and human placental lactogen (HPL) in the mother's blood toward the full term of pregnancy were found to be between 300 and 800 times as high as those in foetal blood. No arteriovenous difference in concentration between the same hormones was recorded from the vessels of the umbilical cord. While the concentrations of progesterone, unconjugated oestriol, and total oestriol in the mother's blood were lower than those in foetal blood, the opposite was true for oestradiol which was lower in foetal blood. Clearly reduced levels of progesterone, unconjugated oestriol, and oestradiol but increased levels of total oestriol were recorded from the umbilical artery, as compared to the umbilical vein. The above findings are intended to encourage thinking about selective penetrability of the placenta, whenever hormone preparations are prescribed in advanced pregnancy.

Female↗
PubMed1985

Prolactin secretion during pregnancy and puerperium: response to metoclopramide and interactions with placental hormones.

Prolactin (PRL) response to an intravenous administration of metoclopramide (10 mg) was examined during normal pregnancy and puerperium. Basal PRL and the metoclopramide-induced increase of PRL increased gradually during pregnancy. This was paralleled by serum estradiol, estriol, and progesterone levels. A positive correlation between serum progesterone and metoclopramide-induced PRL concentrations was found at week 36 of pregnancy. In lactating women, metoclopramide always induced higher increases of PRL than did suckling stimulation on the seventh day postpartum. The PRL responses to suckling and metoclopramide were significantly correlated with each other, but no correlation was found between placental steroid levels throughout pregnancy, PRL levels after parturition, and total milk production during seven days postpartum.

Animals↗
PubMed1999

Maternal endocrine adaptations to placental hormones in humans.

The remarkable endocrine alterations that are characteristic of human pregnancy are attributable to the placenta. In this tissue, steroid and peptide hormones are produced in extraordinary amounts. In addition, the haemomonochorioendothelial placentation of human pregnancy contributes to the unique distribution of products formed in trophoblasts into maternal and fetal compartments. In this review, the partial control exerted by the trophoblast on maternal metabolism is illustrated by the replacement in the maternal compartment of pituitary growth hormone (GH) with the trophoblast's own product, human placental GH. Placental GH differs from pituitary GH by 13 amino acids, has high somatogenic and low lactogenic activities and is secreted by the syncytiotrophoblast in a non-pulsatile manner. This continuous secretion appears to have important implications for the control of maternal levels of insulin-like growth factor I. Placental GH secretion is inhibited by glucose in vitro and in vivo, and is significantly decreased in the maternal circulation in cases of pregnancies with intrauterine growth retardation.

Adaptation, Physiological↗
PubMed1993

Changes in the concentration of alpha-fetoprotein and placental hormones following two methods of medical abortion in early pregnancy.

OBJECTIVE: Measurement of alpha-fetoprotein (AFP) was used to investigate the occurrence of feto-maternal haemorrhage in women undergoing medical abortion. DESIGN: Three groups of women with amenorrhoea of 56 or less days were studied. A control and a mifepristone group had two blood samples taken 48 h apart. Women undergoing medical abortion with gemeprost had two blood samples taken 24 h apart. SETTING: Medical Termination Unit, Simpson Memorial Maternity Pavilion, Edinburgh. SUBJECTS: Three hundred and thirty-five women requesting abortion. INTERVENTIONS: Blood samples taken at 24 h or 48 h apart. MEASUREMENTS AND MAIN RESULTS: The rise in concentration of AFP in plasma was much higher (P = 0.01) in the two groups of women in whom abortion was induced by gemeprost or mifepristone than in control women. Whereas only 5% of women in the control group had a significant rise in AFP, 27% and 33% of women in the mifepristone and gemeprost groups, respectively, had a rise in AFP level which exceeded the 95th centile (> or = 38%). The concentration of hCG rose by 48 h in both control and mifepristone groups. Progesterone remained unchanged, and oestradiol decreased (P < 0.02) in the mifepristone group. By 24 h, there was a significant fall in the concentrations of hCG, progesterone and oestradiol in the group who had aborted after being given gemeprost. CONCLUSIONS: Anti-D prophylaxis must be administered to rhesus negative women to avoid rhesus iso-immunisation.

Abortifacient Agents, Nonsteroidal↗
PubMed2006

Lysyl oxidase interacts with hormone placental lactogen and synergistically promotes breast epithelial cell proliferation and migration.

Lysyl oxidase (LOX), an extracellular amine oxidase, catalyzes the cross-linking of collagen and elastin. LOX has been also shown to play an essential role in promoting the invasive and metastatic potential of breast tumor cells. However, the LOX-interacting factors in these processes are not known. In this study, we identified placental lactogen (PL), a member of the growth hormone/prolactin hormone family, as a LOX-interacting partner using yeast two-hybrid screens. PL is normally only expressed in placental syncytiotrophoblasts, but PL genes are amplified and expressed in a high percentage of invasive ductal breast carcinomas. We confirmed LOX-PL interactions using far Western and solid phase binding assays. In activity assays, PL was not a substrate or inhibitor of LOX. We further demonstrated that PL is expressed in breast tumor epithelial cells and detected LOX-PL interactions by coimmunoprecipitation in invasive breast cancer cells. In MCF-10A normal breast epithelial cells stably expressing LOX, PL, or both, LOX had no effect on cell proliferation, PL alone increased proliferation by 49%, and coexpression of LOX and PL led to a 121% increase in cell proliferation. Unlike in tumor cells, LOX did not induce a more migratory phenotype in MCF-10A cells; nor did PL. However, their coexpression resulted in a 240% increase in cell migration, suggesting that these interactions may be highly relevant to the transition of epithelial cells toward a migratory phenotype during the development and progression of breast carcinoma and a significant role for LOX-PL interactions in epithelial cell behavior.

Breast↗
PubMed2004

Progesterone and placental hormone actions on the uterus: insights from domestic animals.

Progesterone is unequivocally required for maternal support of conceptus (embryo/fetus and associated extraembryonic membranes) survival and development. In cyclic sheep, progesterone is paradoxically involved in suppressing and then initiating development of the endometrial luteolytic mechanism. In cyclic and pregnant sheep, progesterone negatively autoregulates progesterone receptor (PR) gene expression in the endometrial luminal (LE) and superficial glandular epithelium (GE). In cyclic sheep, PR loss is closely followed by increases in epithelial estrogen receptor (ERalpha) and then oxytocin receptor (OTR), allowing oxytocin to induce uterine release of luteolytic prostaglandin F2alpha pulses. In pregnant sheep, the conceptus produces interferon tau (IFNtau) that acts on the endometrium to inhibit transcription of the ERalpha gene and thus development of the endometrial luteolytic mechanism. After Day 13 of pregnancy, the endometrial epithelia do not express the PR, whereas the stroma and myometrium remain PR positive. The absence of PR in the endometrial GE is required for onset of differentiated function of the glands during pregnancy. The sequential, overlapping actions of progesterone, IFNtau, placental lactogen (PL), and growth hormone (GH) comprise a hormonal servomechanism that regulates endometrial gland morphogenesis and terminal differentiated function during gestation. In pigs, estrogen, the pregnancy-recognition signal, increases fibroblast growth factor 7 (FGF-7) expression in the endometrial LE that, in turn, stimulates proliferation and differentiated functions of the trophectoderm, which expresses the receptor for FGF-7. Strategic manipulation of these physiological mechanisms may offer therapeutic schemes to improve uterine capacity, conceptus survival, and reproductive health of domestic animals and humans.

Animals↗
PubMed1995

A homologous radioimmunoassay for ovine insulin-like growth factor-binding protein-2: ontogenesis and the response to growth hormone, placental lactogen and insulin-like growth factor-I treatment in sheep.

Although insulin-like growth factor-binding protein-2 (IGFBP-2) is an abundant IGFBP in fetal and postnatal plasma, its regulation is not yet clearly understood. To address this question in sheep, we purified ovine IGFBP-2 and developed a homologous radioimmunoassay. We have studied its ontogenesis and measured serum concentrations of ovine IGFBP-2 after bovine growth hormone (bGH), ovine placental lactogen (oPL) and IGF-I treatment. Concentrations of IGFBP-2 were high at 125 days of gestation (550 +/- 15 micrograms/l) but fell after birth (P < 0.05) and plateaued after 1 year of age (340 +/- 20 micrograms/l). In lactating ewes, bGH treatment for 7 days significantly reduced (21%; P < 0.05) IGFBP-2 relative to the saline-treated group. Similarly, in neonatal lambs, bGH treatment from day 3 to day 23 of life reduced (P < 0.05) IGFBP-2 by 23% relative to the saline-treated group. oPL had no effect on serum levels of IGFBP-2 in the ewe or the neonatal lamb. In well-fed yearling lambs, treatment with IGF-I reduced IGFBP-2 values by 27% (P < 0.05) relative to control animals. In yearling lambs, reduced nutrition increased plasma IGFBP-2 (41%; P < 0.05). However this increase was abolished by IGF-I treatment. The changes in plasma levels of IGFBP-2 were positively related to changes in IGF-II while there was a negative relationship between circulating IGF-I and IGFBP-2 such that both IGF-I and IGF-II may play a role in the regulation of IGFBP-2 in serum.

Animals↗