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PubMed2003

Porphyromonas gingivalis infection in pregnant mice is associated with placental dissemination, an increase in the placental Th1/Th2 cytokine ratio, and fetal growth restriction.

Our previous animal studies showed that maternal Porphyromonas gingivalis infection in a subcutaneous chamber is associated with hepatic and uterine translocation, as well as systemic induction of maternal inflammatory responses, both of which were associated with fetal growth restriction (FGR). However, P. gingivalis-challenged dams had fetuses with either FGR (2 standard deviations below mean weight of nonchallenged dams) or normal weight. Therefore, the objective of this study was to determine whether maternal infection with P. gingivalis compromises normal fetal development via direct placental invasion and induction of fetus-specific placental immune responses characterized by a proinflammatory Th1-type cytokine profile. P. gingivalis-specific DNA was detected in placentas and fetuses of FGR and normal littermates from P. gingivalis-infected dams. Th1- and Th2-type cytokine mRNA as well as tumor necrosis factor alpha and transforming growth factor beta 2 mRNA were examined in placental tissue by using reverse transcription-PCR to determine Th1/Th2 ratios. For eight litters containing both normal-weight and FGR fetuses, P. gingivalis DNA was detected only in the placentas of FGR fetuses. All fetuses and all amniotic fluid samples from infected and control dams were negative for P. gingivalis DNA. mRNA levels of gamma interferon and interleukin-2 (IL-2) were significantly increased in placentas of FGR fetuses, while expression of IL-10 was significantly decreased in the same group. These data indicate that, in P. gingivalis-challenged dams, within each litter there is placenta-specific translocation of P. gingivalis that results in growth restriction of the targeted fetus, which is associated with a shift in the placental Th1/Th2 cytokine balance.

Animals↗
PubMed1998

Placental antibody transfer: influence of maternal HIV infection and placental malaria.

AIM: To determine the influence of placental malaria, maternal HIV infection, and maternal hypergammaglobulinaemia on transplacental IgG antibody transfer. METHODS: One hundred and eighty materno-neonatal pairs from a Malawian population were assessed. Cord and maternal serum samples were tested for total serum IgG antibody titres using nephelometry, and for specific IgG antibody titres to Streptococcus pneumoniae, measles, and tetanus toxoid antibodies using an enzyme linked immunosorbent assay (ELISA). RESULTS: Multiple regression analyses showed that placental malaria was associated with a decrease in placental IgG antibody transfer to S pneumoniae and measles to 82% and 81%, respectively. Maternal HIV infection was associated with a reduction in IgG antibody transfer to S pneumoniae to 79%; raised maternal total serum IgG titres were correlated with S pneumoniae and measles IgG antibody transfer reduction to 86% and 87%, respectively. No effect was seen with tetanus toxoid antibody transfer. CONCLUSION: The combined influence of placental malaria, maternal HIV infection, and maternal hypergammaglobulinaemia seems to be linked to the low transplacental antibody transfer observed in the Malawian population.

Adult↗
PubMed1987

Placental abruption and placental hemorrhage: correlation of sonographic findings with fetal outcome.

Sixty-nine cases of placental abruption and placental hemorrhage detected with ultrasonography (US) were reviewed retrospectively to determine whether US findings correlate with fetal outcome. Four patients were lost to follow-up, and in the remaining 65 patients fetal outcome included demise in 12 cases (18%), termination of pregnancy in six (9%), premature delivery of a living infant in 15 (23%), term delivery of an infant who was small for gestational age in four (6%), and normal term delivery in 28 (43%). Fetal mortality correlated best with the estimated percentage of placental detachment, but was also significantly (P less than .01) associated with the location (retroplacental) and size (greater than 60 ml) of hemorrhage. Premature labor was associated (P less than .001) only with gestational age at the time of clinical presentation. No sonographic finding was identified as a risk factor for small-for-gestational-age infants. Sonographic findings of placental abruption correlate with fetal outcome, and this information may be useful for guiding obstetric management.

Abruptio Placentae↗
PubMed1998

Formation and retention of cotinine during placental transfer of nicotine in human placental cotyledon.

Maternal smoking during pregnancy causes reduction of fetal breathing movements, an effect attributed to nicotine in fetal blood. Nicotine is metabolized to cotinine which has a long plasma half-life and exhibits slow clearance across membrane barriers. It is also known to activate placental phospholipase-A2-like enzymes, resulting in formation of prostaglandins. Therefore, we studied transport of nicotine in isolated perfused cotyledon of normal human term placenta. The placental cotyledon was perfused with aerated (21% O2, 5% CO2) Krebs-Ringer bicarbonate buffer (pH 7.4, 37 degrees C) containing 2% albumin on both maternal (230 ml, 15 ml/min, 35 mm Hg) and fetal (93 ml, 1.75 ml/min, 70 mm Hg) sides in a closed recirculating system. Nicotine (2 mg) was added to the maternal perfusate; perfusate samples (1 ml) were collected from both sides at regular intervals and analyzed for nicotine and cotinine by high-pressure liquid chromatography. This study gave the following results: (1) In about 60-80 min, 18.6% of the nicotine added to the maternal perfusate was transferred to the fetal perfusate, and the maternal/fetal concentration ratio reached 1.0. These results show rapid placental transfer of nicotine, consistent with its high lipid solubility. (2) Less than 1% is metabolized to cotinine in placenta. The ratio of cotinine concentrations in maternal and fetal perfusates reached 1.0 in about 40 min. These studies were also verified using 14C-nicotine. (3) Maximal reduction in fetal breathing movements occurs at about 30 min, and recovery occurs at 90 min after tobacco smoking by the mother. These observations agree with the rate of placental transfer of nicotine. (4) When nicotine was added on the fetal side, part of it was metabolized to cotinine. However, the maximal concentration of cotinine was twice higher on fetal than on maternal side. These observations suggest that accumulation of cotinine on fetal side may activate prostaglandin formation and trigger spontaneous abortions in pregnant smokers.

Adult↗
PubMed1985

Effects of fetal decapitation upon porcine placental metabolism. Evidence for a fetal influence in placental metabolism.

This experiment was performed to determine if the fetus can influence its placental metabolism. Fetal pigs were decapitated at 45 days of gestation and their placentas compared at 110 days to within litter controls. No histological or histochemical differences were observed. Glycogen levels were elevated in the fetal placenta of decapitated pigs by 107%. Fatty acid synthesis was increased in the fetal placenta of decapitated animals (12.9 +/- 1.5 vs. 3.4 +/- 0.7 nmol acetate units/100 mg/2 h). Fetal decapitation increased fetal placental fatty acid esterification by 43% and oxidation by 125%. The altered lipid metabolism of the fetal placenta was reflected in enzymes associated with substrate utilization (pyruvate kinase and lactate dehydrogenase). Maternal placenta lipogenesis was also altered by fetal manipulation. Leucine conversion to its alpha ketoacid was increased in the fetal placenta of the decapitated pigs (14.8 +/- 1.7 vs. 8.6 +/- 1.4 nmol/100 mg/2 h) indicating amino acid metabolism was affected by this treatment. The ability of an altered fetal endocrinology and metabolism to affect the placental metabolism supports the concept of a fetal influence on placental metabolism.

Animals↗
PubMed1992

Effects of nifedipine on placental blood flow, placental weight and fetal weight in normotensive and spontaneously hypertensive rats.

The effect of nifedipine on placental blood flow was investigated in spontaneously hypertensive rats (SHR) and compared with that in normotensive Wistar Kyoto rats (WKY) by means of the clearance of hydrogen gas generated by electrolysis. The placental blood flow of nifedipine-treated WKY (5, 10 and 25 mg/kg) was significantly (p < 0.05) reduced compared with that of WKY control. On the other hand, the placental blood flow of nifedipine-treated SHR did not change compared with that of SHR control. These data suggest that nifedipine has different effects on placental blood flow in SHR and WKY.

Animals↗
PubMed1991

Transplacental transfer of ritodrine and its effect on placental glucose and oxygen consumption in an in vitro human placental cotyledon perfusion.

Maternofetal transfer of ritodrine and its effect on placental glucose and oxygen consumption were studied using a recycling perfusion of maternal and fetal circulations of an isolated cotyledon of a term human placenta. 3H-labeled ritodrine was introduced into the maternal side of the perfusion system. Transfer was calculated from the linear rise of ritodrine concentrations on the fetal side and was found to be 7.31 +/- 1.02 ng/g placental wet weight/min (SEM) when 1.4 micrograms/ml of ritodrine was used (n = 3) and 14.7 +/- 1.06 ng/g placental wet weight/min when the concentration was 2.8 micrograms/ml (n = 5). The antipyrine transfer rate, 4.1 +/- 0.51 mg/kg/min (n = 8), was used to demonstrate perfusion adequacy and served as an internal standard. Upon computing the mass balance of ritodrine and antipyrine at the end of the experiment, it was found that 17% of ritodrine disappeared from the perfusion system compared to 0.7% of antipyrine (p less than 0.01). The introduction of ritodrine into the perfusion system did not affect placental glucose and oxygen consumption rates of 0.35 +/- 0.01 mumol/g/min (n = 7) and 0.19 +/- 0.013 mumol/g/min (n = 5), respectively.

Antipyrine↗
PubMed2003

Maternal hypothyroidism in the rat influences placental and liver glycogen stores: fetal growth retardation near term is unrelated to maternal and placental glucose metabolic compromise.

Maternal hypothyroidism impairs fetal growth in the rat, but the mechanisms by which this occurs are unknown. Since the fetus derives its glucose supply from the mother, and maternal thyroidectomy may disturb maternal and placental glucose metabolism, we postulated that maternal and/or placental glucose metabolic compromise may contribute to fetal growth retardation in hypothyroid dams. Feto-placental growth, tissue glycogen stores and glucose levels in sera and amniotic fluid were determined in rat dams partially thyroidectomized (TX) before pregnancy and in euthyroid controls. Fetal body weight at 16, 19 and 21 days gestation (d.g.) was related to pre-mating maternal serum total thyroxine (TT(4)) levels; permanent fetal growth retardation occurred in severely (TX(s); pre-mating maternal serum TT(4)<or=16.19 nM) - but not in moderately (TX(m)) - hypothyroid dams. In TX(s) dams, glycogen concentration was elevated in maternal liver and in the fetal side of the placenta at 16 and 19 d.g., and in the maternal side of the placenta at 19 and 21 d.g., despite maternal euglycemia. In contrast, fetal liver glycogen concentration was deficient in TX(m) dams at 19 d.g. and in TX(s) dams at 19 and 21 d.g., and fetal hypoglycemia occurred in TX(s) dams at 21 d.g. Multiple regression analyses indicate that these fetal deficits are strongly associated with the retardation in fetal growth, while the elevated maternal liver and placental glycogen concentrations have no impact on fetal growth near term. The mechanisms by which severe maternal hypothyroidism permanently retards rat fetal growth remain to be determined.

Amniotic Fluid↗
PubMed1990

[Effect of diseases in pregnancy on certain placental functions. Enzymatic systems degrading placental glycogen in pregnancy with gestosis].

Pathways of human placental glycogen degradation either in normal or gestotic pregnancy were examined. Determinations of glycogen phosphorylase served as an index of glycogen cleavage in the phosphorylitic pathway. The activity of hydrolytic route was measured by estimating placental glucoamylase. Samples of placental tissue were obtained after delivery (between the 36th and the 40th week of pregnancy). In placentas derived from gestotic cases elevated activity of phosphorylase A, the decrease in phosphorylase B activity and the rise in glucoamylase were found. It suggests that gestosis may evoke certain impairment of placental glycogen metabolism deteriorating chiefly the glycogen degradation as it may be observed in hypoxic experiments.

Female↗
PubMed1990

[The maintenance of placental circulation--the study on the platelet inhibition activity of placental chorioepithelial brush border membrane].

We studied the platelet aggregation inhibiting activity of human placental syncytiotrophoblast brush border membrane vesicles (BBMV) and obtained the following results. 1. There existed a very strong platelet aggregation inhibiting activity in placental BBMV. The BBMV almost completely inhibited the platelet aggregation induced by ADP, arachidonic acid and ristocetin. 2. There existed a very strong ADP degrading activity (ADPase activity) in the placental BBMV. ADP was quickly decomposed to AMP by BBMV. 3. Placental BBMV inhibited platelet TXA2 (TXB2) production. In the 0.04 mg/ml protein concentration of BBMV, platelet TXA2 production was almost completely inhibited. 4. There existed a very strong platelet aggregation inhibiting activity in solved BBMV. Soluble BBMV almost completely inhibited the platelet aggregation induced by ADP and arachidonic acid but did not inhibit the platelet aggregation induced by ristocetin. 5. ADP decomposing activity and platelet TXA2 production inhibiting activity were separated by anion exchange column chromatography of soluble BBMV. 6. When BBMV was treated with ultrasonic waves to destroy the membrane structure, only the activity inhibiting ristocetin-induced platelet aggregation was markedly decreased.

Adenosine Diphosphate↗
PubMed1988

[Localization of tumor-associated placental protein in human placental tissue and detection in carcinoma cell lines].

Sections of human placental villi tissue and carcinoma cell lines (SMMC-7721, (MGC-803 and Kato-111; were examined using the indirect immunoperoxidase histological technique to further investigate the localization of the tumor-associated placental protein (PP) in human placental tissue and the expression of PP on carcinoma cell lines. PP was prepared from placenta in the first trimester. Placental tissue sections exposed to PP antisera showed a marked staining of the trophoblast cells, especially in syncytiotrophoblast. The strongly stained area was localized to the cell membrane of syncytiotrophoblast. In contrast, the nucleus and the cytoplasm of syncytiotrophoblast were stained weakly. The specific PP antisera also stained the carcinoma cell lines. Among different carcinoma cell lines, the degree of staining of liver carcinoma cell line (SMMC-7721) was higher than that of gastric carcinoma cell lines (MGC-803 and Kato-111). In the carcinoma cell lines the presence of antigen similar to PP suggests that oncogene (one) occur in human trophoblast cells as well as mice trophoblast cells.

Cell Line↗
PubMed2006

Effect of leptin on the regulation of placental hormone secretion in cultured human placental cells.

Placenta is an important source of leptin during pregnancy that contributes to the high plasma leptin levels in pregnant women. Leptin and its functional receptors are synthesized in trophoblast cells that, in turn, secrete gestational hormones supporting a paracrine or autocrine role for leptin in the endocrine activity of the placenta. In the present study we examined the effect of leptin on in vitro release of gestational hormones (human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone, estrogens and testosterone) by human term placental cells in culture. Placentas at term were obtained immediately after delivery from mothers with uncomplicated pregnancies. Progesterone, hCG, hPL, estradiol, estrone, estriol and testosterone levels were measured by different assays in culture media of cells maintained in monolayer culture after incubation for 12, 24, 48 or 72 h with leptin or placebo. Incubation with leptin did not modify hCG, hPL, progesterone, estriol and estrone secretion for any of the doses and times assayed. However, leptin led to a dose-dependent decrease in estradiol release. This effect was observed when treatment with recombinant human leptin spanned from 12 to 72 h. At this time an increase in testosterone levels was observed in leptin-treated cells versus placebo. These results indicate that leptin can be considered a gestational hormone implied in the endocrine function of the placenta, with an important role in control of the production of steroid reproductive hormones in placental cells in vitro.

Cells, Cultured↗
PubMed2004

[Clinicopathological study of intermediate trophoblastic non-tumor lesions: exaggerated placental site and placental site nodule].

OBJECTIVE: To investigate the clinicopathological features of intermediate trophoblastic non-tumor lesions, and to evaluate the position of immunohistochemistry in differential diagnoses. METHODS: Clinical presentation and morphological study of 15 cases of exaggerated placental site (EPS) and 4 cases of placental site nodule or plaque (PSNP) were reviewed. Immunohistochemical stains for hCG, hPL, inhibin-alpha, PLAP, CK18 and Ki-67 were performed. RESULTS: The age of patients ranged from 25 to 40 years with an average of 31.5 years for EPS and 26 to 39 years with an average of 34.3 years for PSNP. Microscopically, EPS was characterized by cords and small sheets of implantation site intermediate trophoblasts infiltrating the endometrium, myometrium and arterial walls. The general histological structures of the endometrium and myometrium were preserved. PSNP was characterized by multiple circumscribed nodular lesions consisting of so-called chorionic-type intermediate trophoblasts and hyaline-like matrix present in the endometrium. Immunohistochemical stainings for hPL and CK18 were positive in the 15 EPS cases. Immunoreactivity for CK18, Inhibin-alpha and PLAP was detected in 4 PSNP cases. The Ki-67 labeling index in 15 EPS cases was low (< or = 5%), while Ki-67 index in 4 PSNP cases was close to 0. CONCLUSIONS: The clinical presentation and pathological features of EPS and PSNP differ from those of trophoblastic tumors (placental site trophoblastic tumor, epithelioid trophoblastic tumor and choriocarcinoma). Immunochemical staining is of great value in their differential diagnoses.

Adult↗
PubMed1985

Preservation of human chorionic gonadotropin and placental lactogen secretion and normal morphology following long-term culture of normal human placental cells.

In order to study the regulation of hCG and hPL secretion during gestation, a system for the preservation of the functional integrity of normal placental cells in long-term culture was established. Normal term placental cells were dispersed with 0.25% trypsin-500 units DNAse I and cultured in a monolayer in Dulbecco's modified Eagle medium with 10% fetal bovine serum. Normal cell morphology, basal hCG and hPL production and hCG responses to dibutyryl cAMP were preserved till 54 days of culture. This model may be useful for the study of long-term regulation of normal placental hCG and hPL synthesis and secretion.

Bucladesine↗
PubMed1995

Simultaneous measurement of 45Ca outflow and human placental lactogen release from placental explants.

Kinetics of 45Ca outflow and human placental lactogen (hPL) release were characterized in human placental explants. Measurements of the rate of 45Ca and [3H]-sucrose (extracellular space marker) outflow from preloaded explants showed that, after a 40 min washout period, the 45Ca effluent radioactivity presumably originated from an intracellular compartment. This view was further supported by the La3+ and temperature sensitivity of the 45Ca outflow. Moreover, the addition of ionomycin as well as an increase in the extracellular Ca2+ or Ba2+ concentration provoked a dose-dependent rise in both the 45Ca outflow and hPL release. There were no systematic temporal analogies between the pattern of 45Ca outflow and hPL release. Taken together, these observations suggest that the stimulation of 45Ca outflow reflects an increased rate of 40Ca entry. The present data also extend previous observations indicating that hPL release can be stimulated by Ca2+ entry. Lastly, the 'in vitro' method described herein allows one to compare rapid changes in hPL release with associated ionic events and can be used to further document the relationships between placental secretory responses and cell calcium metabolism.

Barium↗
PubMed2006

Large-scale preparation and in vitro characterization of biologically active human placental (20 and 22K) and pituitary (20K) growth hormones: placental growth hormones have no lactogenic activity in humans.

Expression plasmids containing DNA sequences optimized for expression in Escherichia coli were prepared encoding human pituitary (hGH-N 20K) and placental (hGH-V 20 and 22K) growth hormones. The proteins were expressed in bacteria, refolded and purified to homogeneity by anion-exchange chromatography on Q-Sepharose according to a unique protocol developed for each protein. The yields from 5l of fermentation culture varied between 400 and 700mg of electrophoretically pure, over 95% monomeric protein. Circular dichroism (CD) analysis revealed similarity of the purified hGHs' secondary structure to that of the pituitary hGH-N 22K, except for hGH-V 20K, in which the alpha-helix content was lower. The purified proteins were stable as a 0.1% sterile solution held at pH 10-11 at 4 degrees C for at least one month. All three purified hGH molecules formed a 1:2 complex with hGH receptor extracellular domain (hGHR-ECD), similar to hGH-N 22K. Binding experiments using hGHR-ECD revealed that the differences between the two 22K variants or between the two 20K variants were not significant, except that hGH-V 20K exhibited slightly lower affinity. Somatogenic activity was tested in vitro using FDC-P1 cell lines. Whereas the bioactivity of 22K hGHs and hGH-N 20K in FDC-P1-9D11 cells stably transfected with hGHR was almost equal and two to threefold higher than that of hGH-V 20K, in FDC-P1 3B9 cells stably transfected with rabbit (rb) GHR, the bioactivity of both 20K analogues was significantly (five to ninefold) lower than that of the 22K hormones. The lactogenic activity measured in heterologous assays (Nb2-11C cells and Baf/3 cells stably transfected with the long form of rabbit prolactin receptor) revealed that the activity of hGH-N 20K was close to that of hGH-N 22K in the Baf/3 cells, but 4.5-fold lower in the Nb2 cells. The activity of hGH-V 22K was ninefold less in Nb2 cells and 55-fold less in Baf/3 cells, whereas hGH-V 20K had no lactogenic activity in either bioassay. In contrast, in a homologous lactogenic assay using Baf/3 LP cells stably transfected with hPRLR, the activity of both placental hGHs was nil and the activity of hGH-N 20K was 4.3-fold lower than that of hGH-N 22K. The latter finding raises the question of whether the lack of intrinsic lactogenic activity in the placental hGHs that dominate during pregnancy has any physiological relevance.

Animals↗
PubMed1987

The effects of insulin-like growth factor-I and insulin on placental lactogen production by human term placental explants.

The effects of insulin-like growth factor (IGF)-I and insulin on placental lactogen production (hPL) by term human placental explants were studied. The hPL content in medium and explant decreased rapidly after first 24 hours of culture. The decrease thereafter was gradual and reached a plateau by day 4 of culture. The decrease of HPL content in placental culture has previously been suggested being due to the depletion of a rapidly secreting preformed pool of hPL. Addition of IGF-I (0.1-10 micrograms/ml) and insulin (1-20 micrograms/ml) stimulated the decreased level of hPL in tissue and medium after 24 hours in culture. IGF-I was 10 times more potent than insulin in stimulating hPL. These findings suggest that IGF-I and insulin effects the production of hPL by placenta. The lower potency of insulin may indicate that the effect of insulin on hPL production is via IGF-I receptor.

Female↗
PubMed1994

Co-localization of placental lactogen-I, placental lactogen-II, and proliferin in the mouse placenta at midpregnancy.

This study was undertaken to determine whether mouse placental lactogen (mPL)-I, mPL-II, and proliferin (PLF) are expressed by the same population of placental giant cells at midpregnancy. Tissue sections from Day 9 of pregnancy were analyzed by double immunofluorescence staining. Sections were stained for PLF by use of a rhodamine-conjugated second antibody, and for mPL-I or mPL-II by use of a fluorescein-conjugated second antibody. All three proteins were present in most of the same giant cells. The distribution of mPL-I and PLF among giant cells in vitro was also examined. When placental cells from Day 7 of pregnancy were cultured for 5 days, > 90% of the cells that immunostained for mPL-I also immunostained for PLF on the first 3 days of culture. Thereafter, the percentage of cells that contained both proteins declined rapidly while the percentage that contained only PLF increased, suggesting continued differentiation of the cells in vitro. These data demonstrate that the same trophoblast giant cells express mPL-I, mPL-II, and PLF simultaneously at midpregnancy, suggesting that their gestational profiles in maternal blood during this period result at least partly from changes in gene expression in one population of cells and not from differentiation of several subsets of giant cells, each expressing only one member of the gene family.

Animals↗