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At least 793 records · Page 44Linked to original sources
PubMed2002

Possible involvement of placental peptidases that degrade gonadotropin-releasing hormone (GnRH) in the dynamic pattern of placental hCG secretion via GnRH degradation.

The presence of an extrahypothalamic gonadotropin releasing hormone (GnRH) in human placenta is well known and this decapeptide is presumed to play an important role in the regulation of the function and growth of human placenta. Immunohistochemistry showed that neutral endopeptidase 24.11 (NEP), a candidate of the responsible enzyme of GnRH degradation, is highly expressed on the cell surface of trophoblasts. Hydrolysis of GnRH by human villi was studied by measuring liberated amino acids using high performance liquid chromatography. The GnRH degrading activity was 1.53 times higher after incubation with the membrane fraction of first trimester villi than that after incubation with the membrane fraction of term villi. Phosphoramidon, a potent inhibitor of NEP, reduced the liberated amino acids to about a half, suggesting that NEP is a responsible enzyme for GnRH degradation. Ubenimex, which can inhibit several aminopeptidases, also reduced the liberated amino acids to about 50 per cent. O-phenanthroline, EDTA, and thiorphan could inhibit GnRH degradation but inhibitors of post proline endopeptidase could not. Furthermore, GnRH degrading activity of the membrane fraction was reduced remarkably after the membrane fraction was immunotitrated by anti NEP and anti placental leucine aminopeptidase (P-LAP) IgG. In conclusion, NEP and P-LAP are responsible enzymes for GnRH degradation in human villi.

Adult↗
PubMed1993

Women with prolactin-producing pituitary adenoma show decreased serum placental lactogen during pregnancy.

Prolactin (PRL), growth hormone (GH), placental lactogen (PL), chorionic gonadotropin (CG), estradiol (OE), progesterone (P4) and sex hormone-binding globulin (SHBG) were measured in serum throughout gestation in 9 women with PRL-producing pituitary adenomas. They had been treated at least 1 year with the dopamine agonist bromocriptine before pregnancy occurred. All women bore healthy babies of normal birthweight. Their PRL levels did not show the successive increase seen in normal pregnancies; serum PRL was unphysiologically increased in all patients up to the 20th week of gestation, whereafter PRL levelled off and fell within the normal range. Serum PL levels were lower in the women with prolactinoma compared to healthy pregnant women, despite normal placental weight. The serum GH levels in the patients determined with an immunoassay based on a monoclonal antibody, were low or nondetectable, similar to healthy pregnant controls. In contrast, high molecular weight GH in serum as determined with a monoclonal antibody which also recognizes PL appeared to be increased in comparison with healthy pregnant women. The serum levels of CG, OE, P4 and SHBG were all within the normal range. These results show that the unphysiological secretion of PRL in pregnant women with PRL-producing pituitary adenomas is associated with decreased serum levels of PL.

Adult↗
PubMed2006

Hormonal regulation of fetal growth.

Fetal growth is a complex process depending on the genetics of the fetus, the availability of nutrients and oxygen to the fetus, maternal nutrition and various growth factors and hormones of maternal, fetal and placental origin. Hormones play a central role in regulating fetal growth and development. They act as maturational and nutritional signals in utero and control tissue development and differentiation according to the prevailing environmental conditions in the fetus. The insulin-like growth factor (IGF) system, and IGF-I and IGF-II in particular, plays a critical role in fetal and placental growth throughout gestation. Disruption of the IGF1, IGF2 or IGF1R gene retards fetal growth, whereas disruption of IGF2R or overexpression of IGF2 enhances fetal growth. IGF-I stimulates fetal growth when nutrients are available, thereby ensuring that fetal growth is appropriate for the nutrient supply. The production of IGF-I is particularly sensitive to undernutrition. IGF-II plays a key role in placental growth and nutrient transfer. Several key hormone genes involved in embryonic and fetal growth are imprinted. Disruption of this imprinting causes disorders involving growth defects, such as Beckwith-Wiedemann syndrome, which is associated with fetal overgrowth, or Silver-Russell syndrome, which is associated with intrauterine growth retardation. Optimal fetal growth is essential for perinatal survival and has long-term consequences extending into adulthood. Given the high incidence of intrauterine growth retardation and the high risk of metabolic and cardiovascular complications in later life, further clinical and basic research is needed to develop accurate early diagnosis of aberrant fetal growth and novel therapeutic strategies.

Animals↗
PubMed1997

Endochondral bone growth during early pregnancy compared with pseudopregnancy in rats.

There are physiological and skeletal changes that occur during pregnancy to accommodate the increased calcium needs of late pregnancy and lactation in the rat. Endochondral bone growth is accelerated during early to midpregnancy, but the endocrine basis of this is not clear. The purpose of this study was to define the role, if any, of placental factors in changes in endochondral growth by comparing changes that occur during pregnancy with pseudopregnancy in the rat. Many hormones change during pseudopregnancy, except placental hormones (e.g., placental lactogens) because a placenta is lacking. Rates of endochondral growth were increased during pregnancy and pseudopregnancy compared to age-matched, unmated controls. There were also increases in body weight in both pregnant and pseudopregnant animals. Since the observed changes occur in both pregnant and pseudopregnant animals, this indicates that endocrine factors other than those secreted by placenta are involved in increased growth during early pregnancy.

Animals↗
PubMed1983

Regulation of immunity in rats by lactogenic and growth hormones.

Antibody formation to sheep red blood cells and the development of contact dermatitis in response to dinitrochlorobenzene are impaired in hypophysectomized (Hypo-X) rats. Rat prolactin, rat growth hormone, bovine prolactin, bovine growth hormone, human placental lactogen and human growth hormone all restored the immunological competence of Hypo-X animals. The possible mechanism of action of these hormones on immune reactions is discussed.

Animals↗
PubMed1994

PACAP-38 positively regulates glycoprotein hormone alpha-gene expression in placental cells.

The human glycoprotein hormone alpha-gene is transcriptionally activated by cAMP in placental cells. We have shown that the novel hypothalamic peptide, pituitary adenylate cyclase activating polypeptide, PACAP-38, significantly stimulates intracellular cAMP levels (12-fold increase; P < 0.001) in JEG-3 choriocarcinoma cells. Regulation of alpha-promoter activity was assessed using both the chloramphenicol acetyl transferase (CAT) and the luciferase (LUC) reporter gene systems. alpha-CAT activity was significantly stimulated by PACAP-38 (4-fold increase; P < 0.05) at 24 h with a similar stimulation being seen with a LUC expression vector. The kinetics of stimulation of the alpha-promoter by PACAP-38 were similar to those seen with 8-Br-cAMP and vasoactive intestinal polypeptide (VIP), a peptide which shares 68% homology with PACAP-38. PACAP-38 also stimulated the production of IL-6 from JEG-3 cells with a time course of response similar to that of alpha-promoter transcription. We conclude that human placental choriocarcinoma cells possess functional receptors for PACAP-38, whose activation enhances cAMP formation, alpha-subunit gene transcription and interleukin-6 (IL-6) production.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Differential effects of maternal ovine placental lactogen and growth hormone (GH) administration on GH receptor, insulin-like growth factor (IGF)-1 and IGF binding protein-3 gene expression in the pregnant and fetal sheep.

The role of placental lactogen (PL) in the regulation of maternal metabolism and fetal growth is not understood. Both PL and growth hormone (GH) have been suggested as possible regulators of mammogenesis. Our aim was to compare the effects of recombinant ovine placental lactogen (oPL) and bovine growth hormone (bGH) on maternal mammary gland development and fetal growth. Pregnant ewes were treated from day 101 to 107 of gestation with twice daily subcutaneous injections of recombinant oPL (n = 7), bGH (n = 8) (0.15 mg/kg live weight/day) or saline (n = 8). On day 108 of gestation, fetal and maternal tissues were collected. The relative abundance of growth hormone receptor (GHR), insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3) mRNA was assessed in mammary gland, maternal liver and heart, and in fetal and placental tissues. There was no detectable change in mammary tissue GHR, IGF-1 or IGFBP-3 gene expression with either bGH or oPL treatment. Maternal administration of bGH, but not oPL, during pregnancy caused an increase in maternal hepatic IGF-1 gene expression (P < 0.005). Treatment with oPL, but not bGH, resulted in a significant increase (P < 0.025) in the relative abundance of fetal hepatic IGFBP-3 mRNA. Maternal hepatic GHR gene expression was not affected by treatment. This study suggests that while bGH treatment of pregnant ewes induces characteristic somatogenic responses, oPL treatment does not have comparable effects. However, oPL may indirectly influence the fetal somatotropic axis by altering fetal hepatic IGFBP-3 production.

Animals↗
PubMed1991

Purification from human pregnancy serum of a low molecular weight mitogen similar to placental lactogen and growth hormone.

Recently, we isolated from the serum of pregnant women a factor that induced rapid proliferation of a lactogen-dependent rat lymphoma cell line (Nb2). This mitogenic factor is reasonably specific to pregnancy, since it was present in serum samples from second trimester as well as term-pregnant women, but not in those of adult men or cycling females. It is unlikely that this mitogenic activity (referred to as pregnancy mitogen [PM]) is due to contamination by classical lactogens, since acetone fractionation of serum yielded a preparation devoid of placental lactogen and prolactin, as determined by radioimmunoassays. Further purification of acetone precipitates from term-pregnant serum by ion exchange chromatography and gel filtration yielded a mitogenic activity with a relative mol wt of approximately 10,000. PM activity in the NB2 cell bioassay was not affected by the presence of prolactin antiserum. However, its activity was immunoneutralized by coincubation with anti-placental lactogen serum and, to a lesser extent, anti-growth hormone serum. It appears that PM was not generated by our extraction procedure, since gel filtration of whole serum also yielded a bioactive fraction of approximately 10 kDa. PM was further purified to homogeneity by high-performance liquid chromatography. Examination of the preliminary amino acid composition of PM revealed differences from that of a bioactive fragment of growth hormone and a corresponding portion of placental lactogen, suggesting that PM could be either a molecular variant of these hormones or a novel protein.

Amino Acids↗