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PubMed1997

Detection of benzo[a]pyrene-DNA adducts in human placenta and umbilical cord blood.

Placenta constitutes a vital organ of exchange between mother and foetus. In addition to this favourable effect for foetal development, placenta indirectly may allow transfer of several maternal blood xenobiotics. Human placenta and umbilical cord blood are interesting models for investigating maternal environment and the metabolism, the bioactivation and the transfer of carcinogens such as polycyclic aromatic hydrocarbons. We used them to assess the effect of a woman's smoking on the foetus. Few studies cover this subject. In pregnant women who have continued to smoke, benzo[a]pyrene compound of cigarette smoke is metabolically activated to diol-epoxide derivative: benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide, ultimate carcinogen (BPDE-I). This derivative is covalently fixed on DNA and gives BPDE-I-DNA adducts. By a competitive immunoassay technique, we determined BDPE-I-DNA adducts in 20 samples of placenta and umbilical cord blood from women who smoked (n = 15) and who did not (n = 10). Tobacco consumption was checked by urinary cotinine determination. In the group of smokers levels of adducts were found in 13 specimens of placenta (from 10 to 60 fmol/50 micrograms of DNA) and 12 umbilical cord blood (from 10 to 22.15 fmol/50 micrograms of DNA) samples. These results indicate that a mother's tobacco consumption is linked to the accumulation of BPDE-I-DNA adducts in the placenta, which are seen in smaller quantities in the umbilical cord blood, probably because of the metabolic capacity of the placenta and the transfer of B[a]P from the mother to the foetus.

Adolescent↗

PubMed2003

Percutaneous treatment of placenta percreta using coil embolization.

PURPOSE: To report the use of embolotherapy to avoid hysterectomy in rare placenta percreta. CASE REPORT: A pregnant 34-year-old woman (gravida 3, para 2) was admitted with premature rupture of membranes and vaginal bleeding in the 32nd week. Prenatal B-mode and Doppler ultrasound revealed marked hypervascularity of the placenta with disruption of the uterine-bladder interface consistent with placenta percreta. Since the patient insisted on uterine preservation, uterus and placenta were left in situ after caesarean section, which was followed by coaxial microcoil embolization of 6 pelvic arteries and postoperative methotrexate administration. Three months later, the patient had severe bleeding from the retained placenta, possibly under the influence of anticoagulation administered for pulmonary embolism. Emergent hysterectomy was performed. CONCLUSIONS: Coil embolization may avoid immediate hysterectomy and reduce peri-delivery blood loss in placenta percreta. However, retained placenta poses a serious risk, even after months, and secondary hysterectomy should be performed as an elective procedure after embolization.

Adult↗

PubMed1990

Immunoelectron microscopic localization of aromatase in human placenta and ovary using microwave fixation.

In this study we investigated the immunohistochemical localization of a unique aromatase, a single protein of 51,000 daltons, in the human placenta and ovary at light and electron microscopic levels. Microwave fixation was adopted for the immunoelectron microscopic study because it is an excellent method for preserving antigenicity and subcellular structures in frozen sections. Tissue samples from four immature human placentas, four full-term human placentas, and two human ovaries fixed in 10% formalin were examined by light microscopy. In addition, tissues from three full-term human placentas and one immature human placenta fixed in 4% paraformaldehyde were examined by electron microscopy. By light microscopy, immunoreactivity for this aromatase was located in the syncytiotrophoblast and a part of the cytotrophoblast of the placenta and in the lutein and granulosa cells of the ovary. Immunoelectron microscopy revealed that the aromatase antigen was localized on the surface of the microvilli, the lateral plasma membrane, and in the endoplasmic reticulum (ER) in the syncytiotrophoblast of the placenta. The positive immunoreactivity in the syncytiotrophoblast ER is consistent with previous results using antibodies for other types of aromatase, whereas the reactivity on the microvilli has not been previously described. The present report describes the fine localization of this unique aromatase in placental and ovarian tissues; its localization on the plasma membranes requires further physiological investigation.

Adult↗

PubMed1977

Placental steriodogenesis in the rat: comparison of normal and giant placentae.

Placental hypertrophy was induced in pregnant rats by daily treatment with estrone (0.5 microng) and progesterone (4 mg) from day 3 through 19 combined with ovariectomy on day 12 of pregnancy. The ratio of basal zone to whole placenta was 47% by weight in these enlarged placentae on day 20 of pregnancy but only 34% in normal placentae. In each case, the basal zone tissue was homogenized and the 10,000 x g supernatant fraction was used for in vitro incubation with [7alpha-3H]pregnenolone as the added substrate. The normal placental tissue synthesized more progesterone and testosterone but less androstenedione and 5alpha-pregnane-3,20-dione than the giant placentae. Utilization of the pregnenolone substrate by the giant placentae was subnormal. Addition of 200 IU of human chorionic gonadotropin (hCG) in vitro to normal basal zone placentae sharply increased the production of progesterone, 17alpha-hydroxyprogesterone, androstenedione and 5alpha-pregnane-3,20-dione. The giant placentage failed to respond to hCG. Thus, steroid-induced hypertrophied placentae in rats do not participate in a compensatory mechanism for steroid hormone production toward pregnancy maintenance.

Androstenedione↗

PubMed1997

Human chorionic gonadotropin-beta gene expression in first trimester placenta.

The hCGbeta gene family contains six genes linked in tandem on chromosome 19 and labeled beta genes 7, 8, 5, 1, 2, and 3. Previous studies on a small number of placentas have indicated that beta gene 5 was the most highly expressed gene during the first trimester of pregnancy, followed by genes 3 and 8. Beta genes 7, 1, and 2 were expressed at very low levels. The purpose of this study was to determine 1) whether this pattern of expression was typical during normal pregnancy by sampling a large number of first trimester placentas, and 2) whether there was a correlation between gestational age and the pattern of hCGbeta gene expression. Total RNA from 27 first trimester placentas varying in age from 6-16 weeks was reverse transcribed into complementary DNA. The complementary DNA was amplified by PCR, and the amount of DNA representative of each hCGbeta gene was quantified by Genescan analysis. In 14 of the 27 placentas, hCGbeta gene 5 accounted for 50% or more of the total beta messenger RNA expressed. Beta gene 3 was expressed at levels ranging from 1-42% of the total, and beta gene 8 expression ranged from 12-32% of the total. Gene 7 expression was less than 3% of the total beta expression in all 27 placentas. Although there appeared to be a trend toward lower expression of beta gene 3 in placentas beyond 10 weeks gestational age, there was no correlation of the pattern of beta expression with placental age. Beta gene expression was also examined in two blighted ova, a spontaneous abortion sample, and a hydatidiform mole as well as in cultured JAR choriocarcinoma cells. With the exception of JAR cells, these abnormal tissues had low levels of gene 3 expression, but these levels were within the range of the patterns observed in normal placentas. These data suggest that it is the total amount of hCGbeta gene expression rather than the expression of individual beta genes that is important for the maintenance of normal pregnancy.

Abortion, Spontaneous↗

PubMed2002

Characterization of iodothyronine sulfatase activities in human and rat liver and placenta.

In conditions associated with high serum iodothyronine sulfate concentrations, e.g. during fetal development, desulfation of these conjugates may be important in the regulation of thyroid hormone homeostasis. However, little is known about which sulfatases are involved in this process. Therefore, we investigated the hydrolysis of iodothyronine sulfates by homogenates of V79 cells expressing the human arylsulfatases A (ARSA), B (ARSB), or C (ARSC; steroid sulfatase), as well as tissue fractions of human and rat liver and placenta. We found that only the microsomal fraction from liver and placenta hydrolyzed iodothyronine sulfates. Among the recombinant enzymes only the endoplasmic reticulum-associated ARSC showed activity toward iodothyronine sulfates; the soluble lysosomal ARSA and ARSB were inactive. Recombinant ARSC as well as human placenta microsomes hydrolyzed iodothyronine sulfates with a substrate preference for 3,3'-diiodothyronine sulfate (3,3'-T(2)S) approximately T(3) sulfate (T(3)S) >> rT(3)S approximately T(4)S, whereas human and rat liver microsomes showed a preference for 3,3'-T(2)S > T(3)S >> rT(3)S approximately T(4)S. ARSC and the tissue microsomal sulfatases were all characterized by high apparent K(m) values (>50 microM) for 3,3'-T(2)S and T(3)S. Iodothyronine sulfatase activity determined using 3,3'-T(2)S as a substrate was much higher in human liver microsomes than in human placenta microsomes, although ARSC is expressed at higher levels in human placenta than in human liver. The ratio of estrone sulfate to T(2)S hydrolysis in human liver microsomes (0.2) differed largely from that in ARSC homogenate (80) and human placenta microsomes (150). These results suggest that ARSC accounts for the relatively low iodothyronine sulfatase activity of human placenta, and that additional arylsulfatase(s) contributes to the high iodothyronine sulfatase activity in human liver. Further research is needed to identify these iodothyronine sulfatases, and to study the physiological importance of the reversible sulfation of iodothyronines in thyroid hormone metabolism.

Animals↗

PubMed2006

Endocrine regulation of human fetal growth: the role of the mother, placenta, and fetus.

The environment in which the fetus develops is critical for its survival and long-term health. The regulation of normal human fetal growth involves many multidirectional interactions between the mother, placenta, and fetus. The mother supplies nutrients and oxygen to the fetus via the placenta. The fetus influences the provision of maternal nutrients via the placental production of hormones that regulate maternal metabolism. The placenta is the site of exchange between mother and fetus and regulates fetal growth via the production and metabolism of growth-regulating hormones such as IGFs and glucocorticoids. Adequate trophoblast invasion in early pregnancy and increased uteroplacental blood flow ensure sufficient growth of the uterus, placenta, and fetus. The placenta may respond to fetal endocrine signals to increase transport of maternal nutrients by growth of the placenta, by activation of transport systems, and by production of placental hormones to influence maternal physiology and even behavior. There are consequences of poor fetal growth both in the short term and long term, in the form of increased mortality and morbidity. Endocrine regulation of fetal growth involves interactions between the mother, placenta, and fetus, and these effects may program long-term physiology.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1995

Expression of human gonadotropin-releasing hormone receptor gene in the placenta and its functional relationship to human chorionic gonadotropin secretion.

Placental GnRH is one of the potential paracrine regulators of hCG secretion from the trophoblasts during pregnancy. Maternal serum hCG levels exhibit an exponential rise during the first 6 weeks of pregnancy, peak at 9-10 weeks, decline to a nadir at 20 weeks, and remain at low levels during the rest of pregnancy. However, the placental content of GnRH does not parallel the time course of hCG secretion, and GnRH messenger ribonucleic acid (mRNA) levels in the placenta remain unchanged during pregnancy. These data do not conform with a simple paracrine mechanism of GnRH as a regulator of hCG secretion. We, therefore, examined the potential variation in GnRH receptor gene expression in the placenta, which may account for the GnRH-mediated dynamic pattern of hCG secretion during gestation. First, we established a functional relationship of GnRH and hCG secretion. Using a placental explant culture system, a dose-response effect of hCG secretion was observed in the placental explant at 9 weeks when treated with GnRH ranging from 10(-9)-10(-7) mol/L. The effect of GnRH was completely blocked by a GnRH antagonist (Nal-Glu). The relative responsiveness of hCG secretion to GnRH stimulation at 10(-7) mol/L was further evaluated in placental explants at 6, 9, and 40 weeks gestation. Whereas the 9-week placenta showed a maximal response (> 300%) relative to the 6-week placenta, there was no response in term placenta. Again, the effects of GnRH on hCG secretion were blocked by Nal-Glu, supporting a receptor-mediated event. Localization of mRNA encoding human GnRH receptor in human placenta at 6, 9, 12, 20, and 40 weeks gestation was established by in situ hybridization. The mRNA signals were present in both cytotrophoblast and syncytiotrophoblast cell layers. Signal intensities varied with gestational ages and were abundant at 6 weeks, peaked at 9 weeks, declined at 12 and 20 weeks, and were undetectable at term. The present study demonstrates, for the first time, that GnRH receptor mRNA is expressed in both cytotrophoblasts and syncytiotrophoblasts and exhibits changes paralleling the time course of hCG secretion during pregnancy. These data provide a mechanistic understanding that the paracrine/autocrine regulation of hCG secretion by placental GnRH is mediated through an increase followed by a decline in GnRH receptor gene expression from the first trimester to term placenta.

Chorionic Gonadotropin↗

PubMed1994

Transfer and uptake of alfentanil in the human placenta during in vitro perfusion.

Alfentanil, a short-acting lipophilic opioid, is used for labor analgesia and cesarean section and may cause neonatal depression. However, direct placental alfentanil transfer has not been studied. We measured placental alfentanil transfer and uptake during in vitro perfusion. Placenta lobules from healthy parturients were perfused with biophase at pH 7.4, 95%:5% O2:CO2. Maternal to fetal (MTF, n = 10) and fetal to maternal (FTM, n = 10) transfer were examined during perfusion with alfentanil 10 ng/mL, antipyrine, and creatinine for 1 h. Thereafter, both MTF and FTM placentas were assayed for alfentanil content (n = 3), or perfused with biophase for 1 h to determine drug washout and then assayed for alfentanil content (n = 3). After the 1 h washout, the remaining MTF placentas (n = 4) were then perfused MTF with high-dose alfentanil 1000 ng/mL to assess saturability of placental transfer. The remaining FTM placentas (n = 4) were then perfused with alfentanil 10 ng/mL in the MTF direction to verify that the same alfentanil transfer characteristics found between placentas were valid when the direction of drug transfer was reversed in the same placenta. Alfentanil was rapidly transferred (< 5 min) across the placenta both MTF and FTM. During MTF transfer, fetal effluent reached a plateau at 2.2 ng/mL between 35 and 55 min, and was unmeasurable 30 min into washout. During FTM transfer, maternal effluent reached a plateau at 1.9 ng/mL at 25-45 min, and was absent after 20-45 min of washout.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗

PubMed2006

Localized expression of histamine H1 receptors in syncytiotrophoblast cells of human placenta.

The previous Northern blot analysis and in situ hybridization studies showed that histamine H1-receptor (H1R) mRNA is expressed in human placenta and suggested that H(1)R plays some roles in the function of placenta in pregnancy. To investigate further, it is essential to show the precise location of H1R in the placenta. In the present study, we investigated H1R expression in human placenta by radioligand binding assay and immunohistochemical study using an antibody against human H1R. Placentas were obtained from normal uncomplicated deliveries. Membranes prepared from the tissue exhibited saturable [3H]mepyramine binding (K(d) = 4.0 +/- 0.6 nM and B(max) = 91.4 +/- 4.9 fmol/mg of protein). Stereoisomers of chlorpheniramine inhibited [(3)H]mepyramine binding; d-chlorpheniramine inhibited more potently than l-chlorpheniramine, K(i) values being 1.1 +/- 0.4 and 270 +/- 170 nM, respectively. The placenta tissues were positively immunostained with anti-H1R antibody only in the region of the syncytiotrophoblast of chorionic villus. The tissues were double stained with anti-H1R antibody and an antibody against human chorionic gonadotoropin (hCG) that is solely expressed in placental syncytiotrophoblast cells. The results showed that H1R and hCG were expressed on the same cells, that is, syncytiotrophoblast cells. These results indicate that H1Rs are specifically expressed in syncytiotrophoblast cells of human placenta organ.

Adult↗

PubMed2003

Effects of oral exposure of bisphenol A on mRNA expression of nuclear receptors in murine placentae assessed by DNA microarray.

Bisphenol A (BPA), a candidate endocrine disruptor (ED), is considered to bind to estrogen receptors and to regulate expressions of estrogen responsive genes. It has also shown evidence of affecting the reproductive, immunological and nervous systems of mammalian embryos. However, the effects of BPA on placentae, a central organ of feto-maternal interlocution, are still unclear. To reveal the mechanisms of BPA effects on placentae in mammals, we compared the mRNA expression of 20 nuclear receptors between placentae of vehicle controls and those of orally BPA exposed pregnant mice by a DNA microarray technique. In murine placentae, mRNAs of 11 nuclear receptors were not detected. However, greater than 1.5 fold changes in mRNA expression of nine nuclear receptors between vehicle control and BPA treated mice were noted. Moreover, remarkable changes in mRNA expression of six non-nuclear receptor proteins were induced by BPA exposure. There were various differences in the effects of BPA on the expression of these mRNAs between the placentae with male embryos and those with female embryos. Such embryo-sex dependent differences are interesting and important pointers to understanding of the endocrine disrupting effect of BPA. The present data indicate that BPA affects the expression of nuclear receptor mRNAs in placentae and may disrupt the physiological functions of placentae.

Administration, Oral↗

PubMed1987

Kinetic assessment of manganese using magnetic resonance imaging in the dually perfused human placenta in vitro.

The transfer and distribution of paramagnetic manganese was investigated in the dually perfused human placenta in vitro (using 10, 20, 100 microM Mn with and without 54Mn) using magnetic resonance imaging (MRI) and conventional radiochemical techniques. The human placenta concentrated 54Mn rapidly during the first 15 min of perfusion and by 4 hr was four times greater than the concentrations of Mn in the maternal perfusate, while the concentration of Mn in the fetal perfusate was 25% of the maternal perfusate levels. Within placentae, 45% of the 54Mn was free in the 100,000g supernatant, with 45% in the 1,000g pellet. The magnetic field dependence of proton nuclear spin-lattice relaxation time (T1) in placental tissue supports this Mn binding. Mn primarily affected the MRI partial saturation rather than spin-echo images of the human placenta, which provided for the separation of perfusate contributions from those produced by Mn. The washout of the Mn from the placenta was slow compared with its uptake, as determined by MRI. Thus, Mn was concentrated by the human placenta, but transfer of Mn across the placenta was limited in either direction. These studies also illustrate the opportunity for studies of human placental function using magnetic resonance imaging as a noninvasive biomarker.

Female↗

PubMed2007

Modulation of apelin and APJ receptor in normal and preeclampsia-complicated placentas.

Apelin is an endogenous ligand of the human orphan receptor APJ. This peptide is produced through processing from the C-terminal portion in the pre-pro-protein consisting of 77 amino acid residues and exists in multiple molecular forms. Although the main physiological functions of apelin have not yet been clarified, it is known that apelin is involved in the regulation of blood pressure, blood flow and central control of body fluid homeostasis in different organs. Since human placenta is a tissue where vasculogenesis, blood pressure and flow are dramatically important to allow a normal embryonic and fetal growth and development, the aim of the present study was to investigate the immunohistochemical distribution of apelin and APJ in normal placentas throughout pregnancy and in preeclampsia-complicated placentas. Specifically, we observed that in normal placentas the expression levels of apelin decreased from the first to the third trimester of gestation in both cytotrophoblast and syncytiotrophoblast cells and in the stroma of placental villi, in contrast with increased expression levels of APJ in the cytoplasm of cytotrophoblast cells and in the cytoplasm of endothelial cells of normal placenta samples. In contrast, in preeclampsia-complicated pregnancies, we observed a very strong increase of expression levels of both apelin and APJ receptor in all the placental compartments, cytotrophoblast, syncytiotrophoblast and stroma with a particular increase in endothelial cells inside preeclamptic placental villi. Our data seem to indicate an important role of apelin and APJ in the regulation of fetal development through a correct regulation of human placenta formation during pregnancy. Moreover, the strong expression levels of apelin and APJ in preeclamptic placentas, suggest their possible involvement in the onset of this pathology.

Adult↗

PubMed1987

Observations on the energy and redox state and protein synthetic rate in animal and human placentas.

The energy and redox states of placentas in newly anesthetized or sacrificed guinea pigs and sheep were compared with that of human placentas immediately after delivery. Subsequently the effect of ischemia was observed in both human and animal placentas. The influence of perfusion, using a fluid containing oxygenated red cells (adult human) was studied in the human placenta. Adenine nucleotide precursors were added to the perfusion fluid in an attempt to improve the energy and redox states and the mixed protein synthetic rate of the tissue. The ATP and lactate concentrations in guinea pig placental tissue taken immediately after nembutal anesthesia were 1.16 and 3.59 mmol kg-1 wet weight respectively. One minute's ischemia caused a fall in ATP to 0.7 and a rise in lactate to 6.5 mmol kg-1. The concentration of ATP in human placental tissue, 30 secs to 3 minutes after delivery of the organ, was 0.52 and of lactate 4.8 mmol kg-1 wet weight, suggesting that some biochemical deterioration had already occurred. A further fall in ATP to 0.21 and rise in lactate to 6.4 mmol kg-1 wet weight took place during 20 mins of ischemia; thereafter the ATP level remained constant while the lactate continued to rise to 11 mmol kg-1 wet weight by 1 1/2 hours. The initial energy charge was similar in both animal and human placentas, 0.8-0.9, and was only reduced during prolonged hypoxia at 37 degrees C. Since the AMP did not rise to the same extent as in other tissues, it is suggested that the Atkinson equation used in the calculation of energy charge may not be applicable to the placenta, and that the most sensitive indication of deterioration in energy status is the swift fall in ATP concentration. Rapid establishment of maternal intervillous perfusion of an isolated lobule of the human placenta using ixygenated RBCS in the perfusion fluid, enabled the ATP and lactate levels to be maintained near to 'in vivo' values during one hour, with a protein turnover rate of 40% day-1, two thirds of that observed 'in vivo' in the sheep. The addition of 1.0-50 microM adenosine to the perfusion fluid improved the energy state of the tissue, but not its redox state nor protein synthetic rate. 1.5 microM inosine in the perfusion medium did not alter the energy state but caused a marked reduction in lactate production.

Adenosine↗

PubMed1988

125I-human epidermal growth factor specific binding to placentas and fetal membranes from various pregnancy states.

Specific binding of 125I-human epidermal growth factor (hEGF) to homogenates of term human placentas and fetal membranes from normal and appropriate for gestational age (N = 20), intrauterine growth retarded (N = 9), twin (N = 11), White class A/B diabetic (N = 12), and large for gestational age (N = 13) pregnancies was measured. In all pregnancy states, placentas bound approximately four times more 125I-hEGF than did fetal membranes (P less than 0.001). There was no significant difference in 125I-hEGF binding to fetal membranes from the various pregnancy states (P greater than 0.05). 125I-hEGF specific binding to placentas from intrauterine growth retarded or twin pregnancies was significantly greater compared with placentas from normal and appropriate for gestational age pregnancies (P less than 0.05). The binding to placentas from pregnancies complicated by White class A/B diabetes or large for gestational age infants, on the other hand, was not significantly different from that to placentas from normal and appropriate for gestational age pregnancies. 125I-hEGF specific binding did not differ between placentas from intrauterine growth retarded or twin pregnancies (P greater than 0.05). Placental and fetal membrane 125I-hEGF binding did not vary with fetal sex, maternal race, placental weight, or gestational age between 37 to 42 weeks (P greater than 0.05). Placental but not fetal membrane 125I-hEGF binding increased with increasing infant weight when appropriate for gestational age and large for gestational age infants were included (P less than 0.05, r = 0.38, N = 32) but not for intrauterine growth retarded, appropriate for gestational age, or large for gestational age infants alone.

Embryonic and Fetal Development↗

PubMed1995

Identification and characterization of a corticotrophin-releasing hormone receptor in human placenta.

Corticotrophin-releasing hormone (CRH) causes vasodilatation in the human fetal-placental circulation and has paracrine actions in placental tissue, suggesting that CRH receptors may be present in the human placenta. We have now identified and characterized placental CRH binding sites and compared them to those described previously in human myometrium and rat pituitary. Radiolabelled ovine CRH binding to placental membranes was pH-, time-, temperature- and divalent cation-dependent and was reversible in the presence of 1 mumol/l unlabelled ovine CRH. Scatchard analysis of placentae delivered vaginally or by elective caesarean section revealed dissociation constants (Kd) of 214.5 +/- 84 pmol/l (N = 8) and 45.4 +/- 23.9 pmol/l (N = 9), respectively. The Kd for caesarean placental binding sites was similar to that of human myometrium (59.6 pmol/l, N = 3) and rat pituitary (82.5 pmol/l, N = 3) receptors. However, in vaginally delivered placentae the CRH binding sites had a much lower affinity (p < 0.05). The receptor densities (Bmax) of vaginally delivered and caesarean-delivered placentae were 28.6 +/- 9.6 and 6.1 +/- 2.8 fmol/mg, respectively (p < 0.05). Chemical cross-linking studies using disuccinimidyl suberate indicated that the molecular weight of the CRH receptor in the placenta and rat pituitary is 75 kD. We conclude that there is a high-affinity population of CRH binding sites in the human placenta that are physicochemically similar to pituitary and myometrial CRH receptors. The CRH receptor properties in the placenta change in response to labour, when CRH levels in maternal blood are highest, suggesting that placental CRH may regulate its receptor.

Adolescent↗

PubMed1984

Development of the main and accessory placentae in the Japanese long-fingered bat, Miniopterus schreibersii fuliginosus.

The placentae of the Japanese long-fingered bat were characterized by their morphological and functional transition from the main placenta to the accessory placentae. The main placenta transformed from an endotheliodichorial to a haemodichorial (one layer of syncytiotrophoblast and one layer of cytotrophoblast cells) condition. Degeneration of the main placenta was accompanied by development of two accessory placentae. These developed on both sides (fetal side) of the main placenta, and subsequently converted from a haemodichorial (two layers of cytotrophoblast cells) to a haemomonochorial condition.

Animals↗

PubMed1977

Feto-maternal amino acid patterns and cyclic AMP in the human placenta with abnormal pregnancies, particularly with SFD.

To clarify the causes of SFD from the view-point of placental function, investigations were made on feto-maternal amino acid circumstances and on how cyclic AMP behaves in the placenta, particularly in relation to the transport of amino acid across the placenta. Amino acids were measured by gas liquid chromatography (hydrogen-flame ion detector), c-AMP by the binding protein method, adenyl cyclase activity by Krishna's method, and proteins by Lowry's method. Results show: (1) The levels of maternal amino acids were indistinctive between the SFD group and the normal pregnancy group. (2) The feto-maternal ratio of amino acid concentrations (f/m ratio) was lower in the SFD group than in the normal control. (3) The level of c-AMP in the placenta was lower in the SFD group than in the control. (4) The lower level of placenta c-AMP in the SFD placenta seems partly attributable to the decreased adenyl cyclase activity. (5) There was a positive correlation (gamma=0.61) between the content of c-AMP in the placenta and the f/m ratio of amino acid concentrations. These findings suggest a decline in placental active transport of acids in SFD; adenyl cyclase and c-AMP in the placenta presumably play a key role in such course.

Adenylyl Cyclases↗