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PubMed1992

Differentiation of the fetal gonad.

Gonadal differentiation may be divided into four stages: pregonadal, indifferent, primary sex differentiation, and secondary sex differentiation. Sertoli cells appear at 6-7 weeks and Leydig cells differentiate at 8 weeks, but in ovaries, primary sex differentiation occurs much later. Testosterone secretion peaks at 12-16 weeks causing male secondary sex development together with the appearance of anti-Müllerian hormone. Fetal testis is able to synthesize and secrete inhibins. Lower circulating luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels in male than in female fetuses at midgestation suggest that the fetal pituitary is already responsive to the gonadal hormones. Placental human chorionic gonadotrophin may regulate testosterone synthesis at midgestation, and both LH and FSH are likely to have some regulatory effect on fetal gonads during the last third of gestation.

Female↗

PubMed1990

Production of mouse placental lactogen-I by trophoblast giant cells in utero and in vitro.

Mouse placental lactogen-I (mPL-I) is the earliest appearing member of the PRL-GH family of placental hormones. Using immunological techniques, we have localized mPL-I both in utero and in vitro to trophoblast giant cells. Detectable amounts of mPL-I were first seen by immunohistochemistry on day 6 of gestation in the mural trophoblast. On day 7 giant cells of the ectoplacental cone also contained mPL-I, and on day 10 giant cells adjacent to both the decidua basalis and decidua capsularis stained positive. By day 12 however, all intra- and extraembryonic tissues were negative. The pattern of mPL-I staining in the placenta is consistent with its reported gestational serum profile. mPL-I was also present in trophoblast giant cells in vitro shortly after attachment and spreading of day 5 blastocysts. Analysis of conditioned medium from blastocyst outgrowths by immunoprecipitation and two-dimensional electrophoresis, and by immunoblotting, identified mPL-I as the major secretory product from the trophoblast, consisting of a group of acidic proteins of 30,000-45,000 Mr. The synthesis and secretion of mPL-I in vitro occurred in a serum-free medium suggesting that production of this hormone is part of an endogenous program of trophoblast differentiation.

Animals↗

PubMed1985

Hormonal regulation of casein synthesis at the end of pregnancy.

Ovariectomy or ovariohysterectomy on day 18 of pregnancy augmented mammary beta-casein content 28 h later. Progesterone injected immediately and 12 h after ovariectomy showed a clear inhibitory effect on casein synthesis. Estrogen induced a significant increase in mammary beta-casein content when injected 12 h after surgery. Treatment with CB-154 to prevent prolactin release did not affect the increase of casein induced by ovariectomy. When CB-154 was injected to ovariohysterectomized pregnant rats, significant reduction of casein synthesis was obtained. According to these findings, rat placental lactogen in the absence of prolactin and progesterone induces beta-casein synthesis. Therefore prolactin, ovarian and placental hormones interplay at the end of pregnancy for full expression of the mammary gland genome.

Animals↗

PubMed1988

Trophoblastic giant cells of the mouse placenta as the site of proliferin synthesis.

Proliferin (PLF) is a PRL-related glycoprotein secreted by a number of mouse cell lines and by minced mouse placenta. To further investigate the hormone-like characteristics of PLF, we have determined the site of PLF synthesis and storage in the placenta and its concentration in blood serum during pregnancy. By immunohistochemical staining and in situ hybridization PLF protein and messenger RNA (mRNA) were localized to the trophoblastic giant cells. Individual cells contained both PLF and placental lactogen II. Trophoblastic giant cells appear to secrete PLF into the circulation since PLF was found at levels up to 5 micrograms/ml in the serum of pregnant mice by RIA and at somewhat lower concentrations in the amniotic fluid. Moreover, the serum concentration of PLF during pregnancy varied directly with the level of PLF mRNA in the placenta and with the number of placentas per animal. These findings are consistent with the hypothesis that PLF is a placental hormone; its function is not known.

Animals↗

PubMed2001

Influence of labor on fetoplacental adrenomedullin concentrations.

OBJECTIVE: Circulating adrenomedullin is increased in pregnancy, and placental and fetal membranes participate significantly in its secretion. Recent studies have suggested a potential role for this peptide in the regulation of fetoplacental circulation and placental hormonal secretion. Because adrenomedullin acts also as a uterorelaxant in rats, this study was designed to investigate whether fetoplacental adrenomedullin production changes with human labor, either at term or preterm. STUDY DESIGN: Eighty pregnant women grouped according to gestational age and presence of labor were studied. Adrenomedullin concentrations in plasma, amniotic fluid, and placental tissue extracts were measured by means of radioimmunoassay and immunohistochemistry. In addition, the ability of amnion and chorion-decidua to secrete adrenomedullin was investigated in vitro. RESULTS: Adrenomedullin concentrations in amniotic fluid were higher in preterm labor, whereas no differences were found in adrenomedullin expression or concentrations in tissues or in maternal and fetal plasma between vaginal delivery or elective cesarean section, both at term and preterm. During term labor (8 patients), maternal plasma adrenomedullin concentration decreased with advancing cervical dilatation, being 173 pg/mL at the beginning of the active stage of labor and 57 pg/mL at the time of delivery. Adrenomedullin concentration in the medium of amnion- and chorion-decidua-cultured cells was higher after vaginal delivery. CONCLUSION: These results suggest that a decrease in adrenomedullin production is not involved in the onset of labor in human subjects but rather that it may play a role other than that of a myometrial relaxant in human parturition.

Adrenomedullin↗

PubMed1980

Placental transfer of steroids: effect of binding to serum albumin and to placenta.

The transfer rates and placental retention of a series of steroids were measured using an in vitro perfusion system of an isolated cotyledon of human placenta. The steroids were added to the maternal inflow and rates of appearance in maternal and fetal outflows were measured, from which data were calculated the transfer rate and placental retention. With a low concentration of albumin (0.01 g/dl) in the maternal and fetal perfusates, transfer rates of diethylstilbestrol and ethynylestradiol were initially low, with considerable retention of the steroids within the placenta. Transfer rates increased with duration of perfusion. With high concentrations of albumin (1 g/dl), placental retention was greatly reduced and transfer rates very rapidly reached high levels. Albumin in the fetal circulation was the effective factor in increasing transfer rate; maternal albumin reduced it. The results with estrone and progesterone were qualitatively similar but not as striking, posssibly because of the large endogenous concentrations of these two hormones. Placental retention of dexamethasone, a more polar steroid that does not bind to placenta and binds poorly to albumin, was low and there was little difference between transfer from low- and high-protein perfusates.

Biological Transport↗

PubMed2000

Leptin production and release in the dually in vitro perfused human placenta.

There is clear evidence that the placenta produces leptin. However, it is still unclear to what extent leptin is released into the maternal and the fetal circulation. The aim of our study was to determine placental leptin release rates into these 2 compartments. In 10 term placentas, using dual in vitro perfusion of an isolated cotyledon, concentrations of leptin, hCG, and human placental lactogen (hPL) were determined in perfusates and in the tissue before and after perfusion. With perfusions lasting 270-840 min, total leptin production was 225 pg/g x min [median; interquartile range (IQR), 76-334 pg/g x min]. The release into the fetal circulation was very low (median, 2.5; IQR, 1.1-5.9 pg/g x min) compared with the release into the maternal circulation (median, 203; IQR, 79-373 pg/g x min) corresponding to 1.6% and 98.4% of net release. Only 0.05% of hPL and hCG were released into the fetal circulation and 99.95% into the maternal circulation, confirming previous results. Release into the fetal circulation correlated significantly with release into the maternal circulation for leptin (r = 0.648; P < 0.05) and hPL (r = 0.721; P < 0.05). Furthermore, release of leptin into the fetal circulation was positively correlated with release of fetal hCG (r = 0.661; P < 0.05). Most of the leptin produced by the placenta is released into the maternal circulation, but compared with other placental hormones (hCG and hPL), a considerably higher proportion of leptin is released into the fetal circulation. These findings may at least partially explain the marked increase in maternal serum leptin levels in pregnancy. The rapid postnatal decrease in leptin levels in both the mother and the neonate is also consistent with the concept of placental origin.

Chorionic Gonadotropin↗

PubMed1994

Expression, purification, and characterization of recombinant rat placental lactogen-I: a comparison with the native hormone.

Rat placental lactogen-I (rPL-I), a member of the PRL/GH gene family, is produced by giant cells in the early trophoblast. The small amount of early placental tissue has limited the purification of rPL-I from this source. To obtain sufficient material for in vitro studies we have used a rPL-I cDNA to express this protein in Chinese hamster ovary (CHO) cells and in these studies have compared the recombinant protein with the native rPL-I. Using an affinity column composed of monoclonal antibody to rPL-I coupled to Sepharose 4B, we have purified rPL-I from four sources: 1) recombinant rPL-I produced and secreted in rPL-I-transfected CHO cells, 2) nonglycosylated recombinant PL-I produced by adding tunicamycin (10 microM/ml medium) to rPL-I-transfected CHO cells, 3) native rPL-I secreted by rat choriocarcinoma (RCHO) cells, and 4) serum rPL-I isolated from day 12 pregnant rats. Analysis by two-dimensional polyacrylamide gel electrophoresis and Western blotting revealed nine subforms with increasing mol wt [approximately 34 kilodaltons (kDa)] and acidic pI for recombinant rPL-I and RCHO-derived rPL-I. Four major species of lower mol wt (approximately 23 kDa) were evident in the nonglycosylated rPL-I, suggesting additional peptide cleavage sites. Serum rPL-I contained four additional forms of higher mol wt (approximately 37 kDa) and more acidic pI. When analyzed by the Nb2 lymphoma cell bioassay, RCHO rPL-I, serum rPL-I, and nonglycosylated rPL-I were equipotent with ovine and human PRL. Recombinant rPL-I was 1.5-2.0 times as active as ovine PRL in the Nb2 assay. A RIA was established for rPL-I. The variant rPL-Iv, displayed nonparallel displacement of [125I]rPL-I from the antibody. There was no cross-reactivity with other pituitary or placental members of the GH/PRL family. Measurement of serum levels of rPL-I by RIA after the injection of recombinant-rPL-I into adult female Sprague-Dawley rats revealed a half-life of 9 min for the recombinant protein compared to 7.8 min for the choriocarcinoma-derived hormone. In conclusion, we have shown that although CHO cells will glycosylate the recombinant protein differently than normal placental cells, the biological properties of our recombinant rPL-I are similar to those of the native, placenta cell-derived hormone.

Animals↗

PubMed1995

The etiopathogenesis of breast cancer prevention.

Breast cancer, the most frequent malignancy diagnosed in women, continues to increase in incidence in all industrialized nations. The fact that this disease becomes incurable once it has spread to regional or distant sites indicates that its complexity is beyond our present level of knowledge. A better understanding of the etiopathogenesis and biology of breast cancer is required in order to develop a rational basis for its prevention and therapy. The observation that early parity reduces the risk of developing breast cancer indicates that reproductive and hormonal conditions might play an important role in its prevention. The elucidation of the mechanisms mediating this protection requires the availability of adequate experimental models. The induction of rat mammary carcinomas with chemical carcinogens has proven to be useful for these purposes, especially since, in this model, full-term pregnancy or treatment of virgin rats with a placental hormone, human chorionic gonadotropin (hCG), prior to the administration of the carcinogen protects the mammary gland from tumor development. Since both pregnancy and hCG treatment induce differentiation of the mammary gland, this process is considered to be essential for the inhibition of the neoplastic process. The possibility of preventing breast cancer by treating young nulliparous females with hormones that mimic a full term pregnancy is of practical interest to the human female population, but it requires a thorough knowledge of the development of the human breast. Our studies indicate that the breast of postpubertal nulliparous women is composed of lobular structures reflecting different stages of development. Type I lobules are the most undifferentiated. Type 2 lobules evolve from the previous ones; they are composed of a higher number of ductular structures per lobule. They progress to lobules types 3 and 4, which are present in the breast during pregnancy and lactation. The type 1 lobule, considered to be the site of origin of ductal carcinomas, predominates in the breast of nulliparous women of all ages. In parous women, the type 3 lobule is the most frequent. Primary cultures derived from breast tissues composed of type 1 lobules express phenotypes of cell transformation not observed in cells derived from type 3 lobules. These data acquire relevance in the light that women with a history of early pregnancy are at a lower risk of developing breast cancer than nulliparous women, an effect attributed to differences in the degree of differentiation of the breast. Pregnancy furthers the differentiation of type 1 lobules to type 3, making them refractory to neoplastic transformation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2005

Increased low-density lipoprotein susceptibility to oxidation in pregnancies and fetal growth restriction.

OBJECTIVE: Atherosis and placental infarction have been observed in pregnancies complicated by fetal growth restriction (FGR). Low-density lipoprotein (LDL) oxidation plays a central role in the pathogenesis of atherosclerosis; therefore, it could be involved in the placental alterations observed in FGR. The aims of the present study were to estimate LDL susceptibility to oxidation in pregnancies complicated by FGR and to evaluate their relationship with fetal growth and placental hormone secretion. METHODS: A cohort prospective study was carried out in 50 women with uncomplicated pregnancies and 55 women with FGR. Blood was drawn at 15, 24, and 32 weeks of gestation. Low-density lipoprotein oxidation was initiated by the addition of CuCl2 and formation of conjugated dienes was monitored. Cholesterol, triglycerides, vitamin E, estradiol, progesterone, and placental lactogen were determined. RESULTS: Women with FGR showed a lag phase (minutes from addition of CuCl2) similar to the control group in the first trimester of pregnancy (85.3 +/- 3.3 versus 81.3 +/- 5.6). But in the second and third trimester, they showed a lower lag phase than the control group: 69.6 +/- 3.6 versus 84.4 +/- 3.5 (P < .05) and 69.9 +/- 3.4 versus 95.6 +/- 3.4 (P < .001). During the third trimester, pregnancies complicated with FGR showed lower levels of estradiol, progesterone, and human placental lactogen than those in the control group. In the third trimester, a positive correlation was found between the lag phase and the birth weight (P = .001) and with the plasma levels of estradiol (P = .002). CONCLUSION: Fetal growth restriction is associated with an increased LDL susceptibility to oxidation, a process that could damage the placenta, leading to alterations in placental endocrine function and fetal weight. Pregnancies complicated by fetal growth restriction show an increased LDL susceptibility to oxidation, a process that may lead to placental dysfunction and growth delay.

Adult↗

PubMed1981

Betamethasone administration to the mother and problems in foeto-placental monitoring.

The administration of betamethasone to the mother in order to accelerate maturation of foetal lungs induces significant modifications in the foeto-placental hormonal secretion. Both the total estriol and unconjugated estriol present a sharp fall in the days immediately following the administration and a rise 10-12 days later, depending on a rebound effect. The HPL levels do not variate except for a progressive and constant rising due probably to better cardiocirculatory maternal condition with, consequently, a higher utero-placental blood-flow. All these phenomena increase when the administration of betamethasone to the mother is repeated more then once. The AA. believe that the sharp fall of the estriol doesn't represent a danger for the foetus being only an effect of maternal and fetal adrenal depression. Consequently the AA. suggest to drive the management during and after the administration of betamethasone to the mother on the basis of other foeto-placental functional tests, as cardiotocography. The results were analysed.

Betamethasone↗

PubMedDate not supplied

Leptin and reproduction.

Leptin, the product of the ob gene, is a small peptide molecule synthesized by white adipocytes with an important role in the regulation of body fat and food intake. Leptin and leptin receptor mRNA were first detected in the brain and hypothalamus but now their ubiquitous presence has been demonstrated. Leptin receptor signal transduction involves the activation of signal transducer and activator of transcription (STAT)-3, a member of the transcription family of proteins. Leptin is regulated by hormones and cytokines, interleukin-1, tumour necrosis factor-alpha and transforming growth factor-beta, linking this molecule with the inflammatory response. In addition, emerging evidence has demonstrated that this molecule is related to reproductive function. This small protein is present in the ovary and decidua, in mature oocytes and during embryonic development and trophoblast invasion. Animal models have demonstrated that leptin-deficient ob/ob mice are sterile; however, fertility can be restored by exogenous leptin. In addition, embryos implanted in STAT-3-deficient mice degenerate rapidly and are the target disruption of STAT-3-provoked embryonic lethality. Leptin acts as a novel placental hormone participating in the control of fetal growth and development. Leptin could be a modulator for invasive features of cytotrophoblast cells. We postulate that leptin may have an autocrine/paracrine role in human implantation and placentation.

Animals↗

PubMed1980

Lack of suppression of lymphocyte MIF production by estradiol, progesterone and human chorionic gonadotropin.

The hypothesis that hormones produced by the placenta contribute to immunosuppression during pregnancy is an attractive one. In order partially to evaluate this hypothesis, we utilized the Migration Inhibition Factor (MIF) Assay, which is an in vitro model of delayed hypersensitivity in that presensitized lymphocytes stimulated by antigen release a glycoprotein (MIF) which inhibits the normal migration of macrophages. The effect of placental hormones on this model of cellular immunity was tested using the direct and indirect MIF assays in pre-immunized guinea pigs. Estradiol (1-50 microgram/ml), progesterone (1-50 microgram/ml) and commercial grade or chromatography-purified hCG (1000-5000 IU/ml) did not affect normal macrophage migration and also failed to suppress production of MIF by guinea pig lymphocytes stimulated with antigen. None of the hormones either enhanced or suppressed macrophage response to preformed MIF. The results indicate that these hormones do not suppress lymphocyte reactivity as assessed by the production of lymphokines or the target cell response to the mediator. The reported effects of steroid hormones and crude hCG on other models of cellular immunity are discussed.

Animals↗

PubMed1992

Anti-LHRH and anti-pituitary gonadotropin vaccines: their development and clinical applications.

Active immunization against hormones involved in the regulation of reproduction is a promising approach to immunocontraception. The hypothalamic peptide, LHRH, controls the synthesis and release of the pituitary gonadotropins, LH and FSH, which regulate gonadal steroidogenesis, sperm production, follicular development and ovulation. Immunizing female primates against LHRH or LH induces infertility, but also disrupts the menstrual cycle. Immunization against the beta subunit of the placental hormone, chorionic gonadotropin (hCG), or its fragment prevents pregnancy without interfering with menstrual cycles or ovulation. hCG vaccines have reached the stage of clinical trials. FSH and LHRH have been tested for immunocontraception in male primates. While active as well as passive immunization against FSH reduced spermatogenesis severely, azoospermia could not be achieved consistently. Immunization against LHRH effectively suppressed spermatogenesis in rats and rabbits. Normal sexual behaviour was maintained by concomitant androgen administration. Fertility was restored when antibody titres declined and no adverse effects were observed. A number of LHRH vaccine preparations are being tested in men in several countries, including the United States. Since the LHRH vaccine reduces serum testosterone levels the first clinical studies involve men with prostate cancer. These trials will be followed by immunization of normal men if the antibody response is sufficient and no adverse effects are observed.

Animals↗

PubMed1993

Expression and regulation of the tumour necrosis factor-alpha gene in the female reproductive tract.

Tumour necrosis factor-alpha (TNF), a potent cytokine originally identified as a product of activated macrophages, is now known to be produced by many types of cells, and has been implicated in regulation of normal tissue homeostasis as well as in cellular differentiation. In humans and some murids, the TNF gene is expressed in ovaries, oviducts, uteri, placentas and embryos. Specific transcripts and proteins have been identified in oocytes, granulosa and theca cells, luminal and glandular epithelial cells, myometrial cells, decidual cells, placental trophoblast, macrophage-like cells and embryonic skin. Both prior and subsequent to implantation, uterine TNF mRNA and protein appear in specific cell lineages in an ordered temporal sequence. This and other findings indicate that transcription of the TNF gene in the uterus is regulated either directly or indirectly by ovarian and/or placental hormones. By contrast, there is as yet no evidence for regulation of this gene by other uterine cytokines such as colony stimulating factor-1 (CSF-1). Although the functions of this pleiotrophic, multifunctional molecule are largely unknown, the findings to date are consistent with the postulate that TNF is involved in gamete development, cyclic changes in the uterus, cancers of the female reproductive tract, placental maturation and embryonic development.

Animals↗

PubMed1982

Stimulation of human chorionic gonadotropin secretion by glucocorticoids.

The effects of glucocorticoids on hormone secretion by human placenta in organ culture were studied. The addition of cortisol resulted in a fourfold increase in human chorionic gonadotropin (hCG) secretion over that in untreated cultures after 144 hours' incubation (P less than 0.05), and a twofold increase in hCG was observed in the presence of cortisone (P less than 0.01). Dexamethasone stimulated hCG secretion in a dose-response manner (r = 0.9542; P less than 0.01). Progesterone, which suppresses hCG under these conditions, decreased the cortisol-enhanced secretion of hCG (r = -0.9794; P less than 0.01). No change in the secretion of human chorionic somatomammotropin was observed, but glucocorticoids increased heat-stable alkaline phosphatase activity (P less than 0.001). The physiologic significance of glucocorticoid effects on placental hormone synthesis is discussed.

Alkaline Phosphatase↗

PubMed2006

Animal models of human placentation--a review.

This review examines the strengths and weaknesses of animal models of human placentation and pays particular attention to the mouse and non-human primates. Analogies can be drawn between mouse and human in placental cell types and genes controlling placental development. There are, however, substantive differences, including a different mode of implantation, a prominent yolk sac placenta, and fewer placental hormones in the mouse. Crucially, trophoblast invasion is very limited in the mouse and transformation of uterine arteries depends on maternal factors. The mouse also has a short gestation and delivers poorly developed young. Guinea pig is a good alternative rodent model and among the few species known to develop pregnancy toxaemia. The sheep is well established as a model in fetal physiology but is of limited value for placental research. The ovine placenta is epitheliochorial, there is no trophoblast invasion of uterine vessels, and the immunology of pregnancy may be quite different. We conclude that continued research on non-human primates is needed to clarify embryonic-endometrial interactions. The interstitial implantation of human is unusual, but the initial interaction between trophoblast and endometrium is similar in macaques and baboons, as is the subsequent lacunar stage. The absence of interstitial trophoblast cells in the monkey is an important difference from human placentation. However, there is a strong resemblance in the way spiral arteries are invaded and transformed in the macaque, baboon and human. Non-human primates are therefore important models for understanding the dysfunction that has been linked to pre-eclampsia and fetal growth restriction. Models that are likely to be established in the wake of comparative genomics include the marmoset, tree shrew, hedgehog tenrec and nine-banded armadillo.

Animals↗

PubMed1996

Effects of pregnant human, nonpregnant human, and fetal bovine sera on human chorionic gonadotropin, estradiol, and progesterone release by cultured human trophoblast cells.

Explant and cell culture methodologies are frequently employed in the investigation of the mechanisms that mediate placental hormone production. Recent reports suggest the presence of unknown regulatory factors in maternal serum that may impact significantly on the regulation of these biosynthetic pathways. The present study, therefore, determined the effects of sera obtained from pregnant women in the second to third trimester (PWS), nonpregnant women (NPWS), and men (MS) as well as commercially prepared FBS on hCG, estradiol, and progesterone release into medium by cultured human trophoblast cells. Placental villous tissue was enzymatically dispersed, and cytotrophoblast cells were purified via density gradient centrifugation and cultured (37 C; 90% air-10% CO2) in DMEM with 10% PWS, NPWS, MS, or FBS. All cytotrophoblast cultures aggregated and progressed to syncytial forms, although cells cultured with PWS exhibited notably larger multinucleated syncytial elements by 48 h in culture than cells cultured with FBS. Significant increases (P < 0.05) occurred in hCG, estradiol, and progesterone release due to the progression of cytotrophoblasts into the syncytiotrophoblast phase in all cultures. The quantity of hCG release was unaffected by serum origin. Cells cultured with human serum released greater (P < 0.05) amounts of estradiol than cells cultured with FBS. Cells cultured with MS released more (P < 0.01) estradiol than cells cultured with either PWS or NPWS, in a ratio to the concentration of endogenous androgen precursor available. Progesterone release was greater (P < 0.01) for PWS-cultured cells than for FBS-cultured cells. Progesterone release by NPWS- and MS-cultured cells was intermediate. Syncytiotrophoblasts cultured with PWS released approximately 3-fold more (P < 0.01) progesterone than syncytiotrophoblasts cultured with FBS and low density lipoprotein cholesterol, although the concentrations of available cholesterol substrate were similar. Culture of cells in steroid-depleted or lipoprotein-depleted PWS or FBS resulted in similar decreases (P < 0.01) in estradiol and progesterone release, respectively. In summary, increased estradiol release by placental cells cultured in intact human serum was attributed to aromatizable androgens, whereas enhanced progesterone release by cells cultured in human serum could be only partially attributed to higher concentrations of low density lipoprotein cholesterol substrate in human serum. Evidence of increased syncytial maturity and progesterone release by PWS-cultured cells may indicate the presence of undefined serum-borne regulators, which is enhanced during pregnancy.

Animals↗