Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLACENTA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2004

Retained placenta in Friesian mares: incidence, and potential risk factors with special emphasis on gestational length.

During the foaling seasons of 1999 and 2000, the incidence of retained placenta in 495 normal parturitions of 436 Friesian brood mares was studied. Retained placenta was defined as a failure to expel all fetal membranes within 3 h of the delivery of the foal. Furthermore, the sex of the foal, month of breeding, sire and dam's sire, age of the mare, and time of day of foaling, were studied as factors that might be associated with retained placenta in Friesian mares after normal foalings, and with gestational length. The analysis was carried out using marginal logistic regression, and mixed linear regression, respectively. The incidence of retained placenta was 54%. Mean length of gestation was 331.6 days. Colts were carried 1.5 days longer than fillies. Mares bred in July-September had a 4-day shorter gestation period (329 days) than mares bred earlier in the year. There was a mare, sire, and dam's sire effect on gestational length, and a mare effect on the occurrence of retained placenta. Mares foaling at 4 and >17 years of age, tended to have a lower incidence of retained placenta than mares foaling at 5-17 years of age. No association was found between the occurrence of retained placenta, and gestational length, sex of the foal, month of breeding, dam's sire, and time of day of foaling. It was concluded that the observed high incidence of retained placenta indicates that the Friesian breed of horses has a higher risk for retained placenta than other breeds of horses.

Animals↗
PubMed2003

Increased oxidative stress in pre-eclamptic placenta is associated with altered proteasome activity and protein patterns.

Analysis of the amount of oxidatively damaged proteins in placenta proteins from normal pregnancies and pre-eclampsia revealed a relative increase of about 30 per cent of damaged proteins in pre-eclamptic placenta. Previous work has demonstrated that these cell- and tissue-damaging oxidatively stressed proteins are metabolized particularly by the 20S proteasome. Evaluation of the proteasomal activity revealed a significantly reduced proteasome function in pre-eclamptic placenta by about 30 per cent, suggesting that the accumulation of oxidatively damaged proteins in pre-eclampsia is associated with reduced proteasomal activity. To investigate these effects at molecular levels, separation of placental proteins by two-dimensional SDS-PAGE and subsequent anti-proteasome Western blot revealed several sets of approximately 20 kDa and 30 kDa protein subunits in normal placenta which appear at low or undetectable expression levels in pre-eclamptic placenta. Control Western blots against the placenta protein 14 (PP14) demonstrated equal loading and no significant differences in the PP14 protein patterns. These data suggested that alteration of the multifactorial proteasomal protein complex in pre-eclamptic placenta is accompanied by reduced metabolization of oxidatively damaged proteins. Consequently, the accumulation of these damaged proteins in the placenta may be associated with metabolic interference and thus contribute to certain developments of pre-eclampsia. Silver staining of the two-dimensional SDS-PAGE revealed a variety of acidic proteins in the range of 20 kDa and 45 kDa, respectively, which are differentially expressed in normal and pre-eclamptic placenta and thus provide further analytic potential for metabolic interference.

Carbon Dioxide↗
PubMedDate not supplied

An ultrastructural and ultrahistochemical study of the human placenta in maternal essential hypertension.

An electron-optical study of the placenta in essential hypertension indicates that the morphological changes seen in this disease are qualitatively very similar to those found in placentae from pre-eclamptic women: these changes are accentuated if pre-eclampsia is superimposed on essential hypertension. It is therefore suggested that the abnormalities seen in placentae from hypertensive women are due solely to ischaemia. The extent and degree of ischaemic damage suffered by the placenta is essential hypertension were, however, much less marked and extensive than in placentae from pre-eclamptic patients whilst in placentae from cases of essential hypertension complicated by pre-eclampsia there was less evidence of ischaemic damage than in placentae from cases of pre-eclampsia or comparable severity developing in previously normotensive women. It is suggested that the placenta is able to adapt to a state of chronic ischaemia in a manner that it is not able to do in late onset ischaemia and that the adaptive mechanisms adopted not only limit ischaemic damage but also afford protection to the placenta against the effects of superimposed pre-eclampsia.

Acid Phosphatase↗
PubMedDate not supplied

Histochemical and quantitative biochemical changes in mucopolysaccharides of the term placenta of the diabetic rat.

Full-term placentae of rats with streptozotocin-induced diabetes were analysed histochemically and biochemically for changes in mucopolysaccharide content. The experimental diabetes induced severe cystic degeneration in the spongiosa zone of the placenta and this was accompanied by extracellular deposition of hyaluronate and neutral polysaccharides. The labyrinth zone was affected to a lesser extent. Biochemical analysis also revealed quantitative differences in the total contents of mucopolysaccharides (MPS) between the two zones of the placenta in both diabetic and normal placentae. The spongiosa had a higher total mucopolysaccharide content than the labyrinth. Polysaccharides of low molecular weight were always predominant. The amount of hyaluronate exceeded the quantitites of sulphated mucopolysaccharides which were found in relatively small amounts in both placental zones. In diabetic placentae there was a two- to threefold increase, which was more pronounced in the spongiosa. The increase was observed among all types of MPS. A close correlation between the accumulation of MPS in the placenta and the degree of maternal hyperglycaemia was found. The placentae of the three streptozotocin-resistant animals showed neither histological nor biochemical changes. It is suggested that the accumulation of MPS in the diabetic placenta might be a consequence of a shift in carbohydrate metabolism induced by hyperglycaemia or a persistence of the fetal metabolic features as a part of a retarded maturational process of the placenta.

Animals↗
PubMed1996

TNF alpha concentrations and mRNA expression are increased in preeclamptic placentas.

UNLABELLED: Tumor necrosis factor-alpha (TNF alpha), a cytokine produced mainly by macrophages, is involved in immunoregulation, the modulation of cell growth and differentiation, as well as in the induction of oxygen free radicals. In preeclamptic placentas, lipid peroxides are increased as compared to normal placentas. If TNF alpha was abnormally increased in preeclamptic placentas, it might contribute to the increased oxidative stress and the formation of lipid peroxides. We hypothesized that TNF alpha levels would be higher in preeclamptic than in normal placentas. We determined: (1) the levels of TNF alpha protein in whole placental tissue; (2) the concentrations of TNF alpha protein and lipid peroxides in the medium after 48 h of incubation of whole placental villi; (3) mRNA expression of TNF alpha. Placental TNF alpha protein levels were measured by ELISA, lipid peroxides by a spectrophotometric method specific for peroxides, and TNF alpha mRNA expression by RT-PCR. RESULTS: (1) TNF alpha tissue levels were significantly higher in preeclamptic than in normal placentas, P < 0.05. (2) Concentrations of both TNF alpha and lipid peroxides were higher in the incubation medium of preeclamptic than normal placentas, P < 0.05. (3) TNF alpha concentrations in the incubation medium were positively correlated with lipid peroxide concentrations, r = 0.608. (4) TNF alpha mRNA was expressed in preeclamptic placentas, but not in normal placentas. CONCLUSIONS: TNF alpha protein concentrations and mRNA expression are higher in preeclamptic than normal placentas and this is associated with increased lipid peroxidation.

Enzyme-Linked Immunosorbent Assay↗
PubMed2004

Implantation site intermediate trophoblasts in placenta cretas.

Placenta cretas are defined as abnormal adherences or ingrowths of placental tissue, but their pathogenetic mechanism has not been fully explained. During histologic examination of postpartum uteri, we noticed that the number of implantation site intermediate trophoblasts was increased in the placental bed of placenta cretas. To validate our observation and to address the pathogenetic role of implantation site intermediate trophoblasts in placenta cretas, we examined postpartum uteri with placenta cretas (n=34) and noncretas (n=22), obtained from Cesarean or immediate postpartum hysterectomy specimens. Using antibody to CD146, a marker for implantation site intermediate trophoblasts, we found that placenta cretas had significantly thicker layer of implantation site intermediate trophoblasts (2300+/-1200 mum) than noncretas (1500+/-1200 microm, P<0.025). We also observed that the confluent distribution of cells was more frequent in placenta cretas (97%) than noncretas samples (45%, P<0.001), and that the total number of implantation site intermediate trophoblasts within the superficial myometrium of the placental bed was significantly higher in placenta cretas than noncretas. Using antibodies to Ki-67, Bcl-2 and cleaved caspase-3 to determine the proliferative index and apoptotic rates of implantation site intermediate trophoblasts, we found that they were close to zero in both groups and did not differ significantly. These findings suggest that the increased number of implantation site intermediate trophoblasts observed in placenta cretas may be related to the pathogenesis of placental ingrowth, but the mechanism by which the increase in implantation site intermediate trophoblasts causes placenta cretas remains to be clarified.

Adult↗
PubMed2001

A novel untranslated 'exon H' of the human choline acetyltransferase gene in placenta.

To investigate the existence of 5'-region(s) of human choline acetyltransferase (hChAT) mRNA in placenta we analyzed the presence or absence of ChAT 5'-untranslated regions (UTR) in human neuronal and non-neuronal cells. Total RNA from human spinal cord, placenta, cultured choriocarcinoma JEG-3 and neuroblastoma CHP126 and MC-IXC cells was reverse transcribed and used for polymerase chain reaction amplification (RT-PCR). We used a sense primer located in the 5'-flanking region, in the previously defined intronic sequence and an anti-sense primer located in the common coding exon 2 of the hChAT gene. An amplified product of 567 bp in size was obtained only in human placenta and in JEG-3 cells whereas it was absent in spinal cord, CHP126 and MC-IXC cells. It was designated 'H-type' of ChAT mRNA. Whereas CHP126 produced the R- and N-type of ChAT mRNAs, no transcript of the N-and R-type was detected in JEG-3 and human placenta. In addition, CHP126 and JEG-3 cells and placenta showed the expression of the M-type of ChAT mRNA. The identity of the amplified 567 bp product (H-type) was confirmed by Southern hybridization and sequencing. The nucleotide sequence of the amplified fragment in placenta revealed the existence of a previously unknown type of ChAT mRNA produced by alternative splicing. Using primer extension we further determined the transcription initiation site of the H-type hChAT mRNA in placenta. These results demonstrate the expression of a novel ChAT mRNA isoform in human placenta in addition to the M-type. These data may be possibly explained by the presence of a placenta specific promoter in the ChAT gene, which might be the proximal promoter P1.

Amino Acid Sequence↗
PubMed1999

Human carboxylesterases in term placentae: enzymatic characterization, molecular cloning and evidence for the existence of multiple forms.

The placenta is a temporary organ that is known to metabolize numerous endogenous and xenobiotic compounds. Carboxylesterases represent a family of enzymes which hydrolyse a variety of esters, amides and thioesters. Many studies have demonstrated that carboxylesterases are widely distributed among mammalian tissues, but little is known about these enzymes in the placenta. The present study was conducted to establish the kinetic parameters of placental carboxylesterases toward several p -nitrophenol and 1-naphthol esters, and to establish the molecular basis for these enzymes in the placenta. The enzymatic rate of the hydrolysis of 1-naphthylacetate and carboxylic esters of p -nitrophenol as a function of substrate concentration (0.01-1.00 m m) was examined with human placental microsomes pooled from six placentae. Data from these studies yielded a linear Lineweaver-Burk plot with each substrate examined. K(m)values for these substrates ranged from 92 to 370 microm, and V(max)values ranged from 85 to 170 nmol/mg/min. These results suggest that each substrate is hydrolysed by a single enzyme, or enzymes that are kinetically indistinguishable, or that one of them is dominant. Microsomes from all individual placentae contained esterase activity toward all four substrates, and exhibited a one- to three-fold variation. The activity toward p -nitrophenylacetate correlated well with the activity toward 1-naphthylacetate (r(2)=0.957). In contrast, the activity toward p -nitrophenylbutyrate correlated poorly with the activity toward 1-naphthylacetate (r(2)=0.121). These results suggest that placental microsomes have more than one carboxylesterase activity. Screening of a placental cDNA library with gene-trapping hybridization resulted in the isolation of three distinct cDNAs, designated PCE-1, PCE-2 and PCE-3. PCE-1 and PCE-2 have a significant sequence identity (approx 99 per cent) with liver carboxylesterases hCE and hCE-2, respectively. PCE-3 has a 96 per cent sequence identity with hCE but only at the first 874 nucleotide of the 5' end. The rest of the 1396 nucleotides of the 3' end exhibit no significant sequence identity with any known mammalian carboxylesterases. A probe derived from the 3' end of PCE-3 detected an approx 2.2 kb messenger transcript, the size of a regular carboxylesterase. However, the entire PCE-3 cDNA has multiple internal stop codons and encodes only 269 amino acids; half the size of a regular carboxylesterase. Northern blotting experiments detected the transcripts coding for PCE-1, PCE-2 or PCE-3 in all placentae, and the levels of these messengers showed an approx six-fold individual variation. Placenta 6 had the highest activity toward all four substrates, and highest levels of the messengers for PCE-1, PCE-2 and PCE-3. In contrast, placenta 1 had relatively high levels of messengers for PCE-1 and PCE-2, but the activity toward these four substrates was only moderate. These results suggest that a discrepancy between the messenger level and the enzyme protein exists or that there are other as yet unidentified carboxylesterase(s) in the placenta which contribute to the hydrolytic activity. Carboxylesterases are known to involve the detoxication and metabolic activation of various drugs, environmental toxicants and carcinogens. Therefore, placental carboxylesterases have both pharmacological and toxicological significance in the development of the fetus.

Amino Acid Sequence↗
PubMedDate not supplied

Sonographically thick placenta: a marker for increased perinatal risk--a prospective cross-sectional study.

The aim of this study was to determine placental thickness by ultrasound examination throughout pregnancy and establish the correlation of sonographically thick placenta with perinatal mortality and morbidity. Placental thickness was determined by routine sonographic examination throughout pregnancy in 561 normal singleton pregnancies. Thick placenta was determined as placenta that was above the 90th percentile. Gravidae between 20-22 weeks' gestation (n=193) and 32-34 weeks (n=73) were then divided into two groups according to placental thickness. The study group consisted of 44 gravidae with thick placenta. The control group included 151 gravidae with placental thickness between the 10th and 90th percentile. A comparison of perinatal mortality and morbidity rates as well as the incidence of small and large for gestational age neonates was conducted.A linear increase of placental thickness was found to correlate with gestational age throughout pregnancy. No statistical differences were observed between the two groups with regard to obstetrical variables such as maternal age, parity and gestational age at delivery. No correlation was found between placental thickness and maternal age or parity. The incidence of perinatal mortality was significantly higher among gravidae with thick placentae (6.82% versus 0.66 per cent, P=0.037, 95 per cent confidence interval 1.71-70.29). Birthweight at term was found to be above 4000 g in 20.45 per cent of the thick-placenta group as compared to 5.3 per cent in the control group (P=0.001, 95 per cent CI 2.08-13.85), and birthweight of less than 2500 g was found in 15. 9 per cent of the thick-placenta group as compared to 7.3 per cent in the control group (P=0.03, 95 per cent CI 1.11-8.14). The incidence of fetal anomalies was 9.1 per cent in the thick-placenta group and 3.97 per cent in the control group (not significant). Sonographically thick placenta is associated with increased perinatal risk with increased mortality related to fetal anomalies and higher rates of both small for gestational age and large for gestational age infants at term.

Birth Weight↗
PubMed2003

Placenta previa in singleton and twin births in the United States, 1989 through 1998: a comparison of risk factor profiles and associated conditions.

OBJECTIVE: The purpose of this study was to compare risk factor profiles for placenta previa between singleton and twin live births. STUDY DESIGN: This cohort study was based on United States natality data files (1989 through 1998) and comprised 37,956,020 singleton births and 961,578 twin births. Women who were diagnosed with placenta previa were included only if they were delivered by cesarean delivery. Risk factors for placenta previa that were examined included sociodemographic (age, gravidity, education, marital status, and race), behavioral (prenatal care, smoking, and alcohol use), previous preterm birth, and medical and obstetric factors. Effect modification between maternal age and gravidity and the dose-response relationship with number of cigarettes smoked/day on placenta previa risk were also evaluated. RESULTS: The rate of placenta previa was 40% higher among twin births (3.9 per 1,000 live births, n = 3,793 births) than among singleton births (2.8 per 1,000 live births, n = 104,754 births). Comparison of risk factors for placenta previa between the singleton and twin births revealed fairly similar risk factor profiles. Compared with primigravid women <20 years old, the risk for placenta previa increased by advancing age and by increasing number of pregnancies among both singleton and twin births. The number of cigarettes smoked per day also showed a dose-response trend for placenta previa risk in the two groups. CONCLUSION: The increased rate of placenta previa among twin births underscores the need to monitor carefully such pregnancies with heightened suspicion and awareness for the development of this condition.

Adult↗
PubMed2003

Placenta previa: neonatal death after live births in the United States.

OBJECTIVE: The purpose of this study was to describe neonatal mortality rates among live births that were complicated by placenta previa in the United States. STUDY DESIGN: This was a population-based retrospective cohort study of 1997 United States singleton live births. Neonatal deaths among pregnancies that were complicated by placenta previa were compared with deaths among pregnancies with no placenta previa. Adjusted and unadjusted hazard ratios were generated from a proportional hazards regression model. RESULTS: Of 3,773,369 live births, 9656 were complicated by placenta previa (2.6 cases per 1000). Among cases of placenta previa, 114 neonatal deaths occurred (11.8 per 1000) versus 14951 (4 per 1000) among non-placenta previa neonates (P <.0001). The adjusted relative risk of death was three times higher among placenta previa neonates (hazard ratio, 3.06; 95% CI, 2.40-3.94). Placenta previa-related death was mediated through preterm delivery rather than small for gestational age. CONCLUSION: Placenta previa triples the rate of neonatal mortality, which is mediated mainly through preterm birth.

Adult↗
PubMed2002

Expression and regulation of calcitonin gene-related Peptide receptor in rat placentas.

Calcitonin gene-related peptide (CGRP), one of the most potent vasodilators known, exerts its biological action by interacting with its receptors. Recent reports suggest the existence of two types of CGRP receptors, CGRP-A and CGRP-B. The current study was designed to examine whether CGRP-B receptors are present in the rat placenta, and if they are, whether they are modulated by gestational age and by sex-steroid hormones. Placentas were obtained from timed pregnant Sprague-Dawley rats that were killed on Days 17-21 and 22 before and during labor (n = 6 for each gestational age). In addition, placentas were also obtained from pregnant rats injected with progesterone (P(4); 4 mg per rat per day s.c. on Days 20-22), antiprogesterone RU-486 (10 mg/rat s.c. on Day 17), 17beta-estradiol (5 micro g/rat s.c. on Day 17), and antiestrogen ICI 182780 (0.3 micro g/rat s.c. on Day 17). Results showed that first, immunoflourescent staining of rat placentas using monoclonal anti-CGRP-B receptor antibody revealed the presence of CGRP-B receptors in the labyrinthine layer of the placenta, specifically to the trophoblast and blood vessel endothelium and underlying smooth muscle cells. The intensity of staining was lower in placentas obtained during labor. Second, a single band of 66 kDa, reactive to CGRP-B receptor antibody, was obtained in Western blotting of the rat placenta; third, densitometric analysis of protein bands showed that CGRP-B receptors were increased from Day 17 to Day 22, with maximal levels obtained on Day 22 before labor, which was 10 times higher than that of Day 17 (P < 0.01); fourth, expression of CGRP-B receptors in rat placenta decreased during labor (8% vs. 100% on Day 22 before labor, P < 0.01); fifth, P(4) given during Days 20-22 attenuated the fall in placental CGRP-B receptors at term labor; sixth, RU-486 given on Day 17 of gestation significantly decreased expression of placental CGRP-B receptors (18% vs. 100% in controls at 6 h, P < 0.01); seventh, a significant decrease in CGRP-B receptor expression was noted 48 h after estrogen administration; and eighth, ICI 182780 treatment on Day 17 increased placental CGRP-B receptors (152% vs. 100% in control at 48 h, P < 0.01). These results indicate that CGRP-B receptors are present in rat placenta and that receptor levels are higher with gestational age and lower at term labor. Progesterone stimulated and estrogen inhibited placental CGRP-B receptor expression. Thus, elevations in placental CGRP-B receptors in late pregnancy could play a role in increasing blood flow through the fetoplacental unit associated with rapid fetal growth during late gestation.

Animals↗
PubMed1998

Vascular anatomy of monochorionic placenta in relation to discordant growth and amniotic fluid volume.

The objective of this study was to determine the chorionic plate vascular anatomy of the monochorionic (MC) placenta in relation to the discordance in fetal growth with or without disparity in amniotic fluid volume. In 58 MC placentae, anastomoses were delineated by dye-contrast injection under optimal physiological conditions. Thirty-two pregnancies were complicated by twin-twin transfusion syndrome (TTTS) (n = 32), of which 16 placentae were from severe disease. Ten pregnancies with fetal growth discordance of >20% and with a normal amniotic fluid index (AFI) were also studied. Sixteen uncomplicated MC pregnancies were used as controls. Severe TTTS placentae (median, m 1; range, r 0 to 2) had significantly fewer anastomoses than those from mild disease (m 2; r 1 to 4; P < 0.01), discordant growth (m 3; r 2 to 6; P < 0.001) and controls (m 5; r 2 to 8; P < 0.001). Placentae from severe TTTS had a single unidirectional deep arteriovenous anastomosis, while milder cases, in addition, had a < or = 1 mm bidirectional superficial arterioarterial (n = 9) or venovenous (n = 6) -type shunts. Multiple arteriovenous anastomoses with a paucity of superficial anastomoses were detected in discordant growth placenta. In contrast, control placentae had multiple shunts which were symmetrical in number, type and size both overall and per placenta. The subchorionic distance in severe TTTS and discordant growth placenta were comparable (m 3.5 cm; r 1.6 to 5.8 cm versus m 3.6 cm; r 2.5 to 5.7 cm), but were greater than the mild disease (m 2.5 cm; r 1.2 to 3.8 cm; P < 0.01) and control groups (m 1 cm; r 0.5 to 2.4 cm; P < 0.001). The perinatal mortality in severe TTTS (57%) was higher than that in the mild TTTS (17%) and growth discordant groups (15%). The paucity of superficial anastomoses with presence of solitary or multiple arteriovenous anastomoses is likely to be associated with severe TTTS and fetal growth discordance of >20% respectively. In contrast, in mild TTTS additional superficial arterioarterial or venovenous channels are present along with single deep arteriovenous anastomoses.

Amniotic Fluid↗
PubMed1997

Increase in the relative level of type V collagen in the placentae of patients with pre-eclampsia.

To obtain some insight into the extracellular matrix in the human placenta, we investigated the composition of collagens purified from the placentae of patients with pre-eclampsia and compared it with normal placentae. Collagen was extracted from the placentae of both normal and pre-eclampsia pregnancies during the third trimester. The relative amounts of various collagens were evaluated by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. The ratio of the intensity of the band corresponding to the alpha 1 (III) chain with that of the alpha 1 (I) chain in placentae of pre-eclampsia was significantly lower than in normal placentae (P < 0.05). In contrast, the ratio of the intensity of the band corresponding to the alpha 1 (V) chain with that of the alpha 1 (I) chain in placentae of pre-eclampsia was significantly higher than in normal placentae (P < 0.05). The results suggest that an increased level of type V collagen relative to type I collagen in the placentae of pre-eclampsia might be closely associated with the disturbance to trophoblastic cell functions and the supply of nutrients to the developing fetus necessary for the maintenance of pregnancy.

Adult↗
PubMed1991

Different combinations of regulatory elements may explain why placenta-specific expression of the glycoprotein hormone alpha-subunit gene occurs only in primates and horses.

Expression of the glycoprotein hormone alpha-subunit gene occurs in the pituitary of all mammals but in placenta of only primates and horses. In humans, two different elements, termed upstream regulatory element (URE) and cAMP response element (CRE), are required for placenta-specific expression of the alpha-subunit gene. The URE binds a protein unique to placenta whereas the CRE binds a ubiquitous protein. Comparative analysis of the promoter-regulatory region of the alpha-subunit gene from a number of mammals indicates that a functional URE has been retained and suggests the potential for placenta-specific expression. Indirect evidence also indicates that the URE-binding protein has been conserved, even in placenta from mammals that fail to express the alpha-subunit gene. Lack of expression of the alpha-subunit gene in placenta of rodents and cattle can be traced to a single nucleotide change that renders the CRE-like sequence of these genes incapable of binding the protein that confers responsiveness to cAMP. In contrast, although expression of the alpha-subunit gene occurs in horse placenta, the promoter-regulatory region lacks a functional CRE but appears to retain a functional URE. This suggests that either a different accessory element and cognate protein interacts with the horse URE to provide placenta-specific expression or that a completely different set of regulatory elements is required for placenta-specific expression in horses.

Animals↗
PubMed1999

Previous cesarean section and abortion as risk factors for developing placenta previa.

OBJECTIVE: To determine the risk of subsequent occurrence of placenta previa in women with a history of previous cesarean sections and/or spontaneous and induced abortions. METHODS: A retrospective analysis of all single gestation deliveries at National University Hospital of Singapore from 1993-1997 was done. Women with placenta previa were identified by clinical or ultrasonographic diagnosis. RESULTS: Of the 16,169 singleton deliveries, 164 women (1.0%) had placenta previa. Women with placenta previa had a significantly higher incidence of previous cesarean sections (p < 0.001). Among the 164 women with placenta previa, women with 1, 2, and 3 previous cesarean sections had 2.2 (95% CI 1.4, 3.4), 4.1 (95% CI 1.9, 8.8) and 22.4 (95% CI 6.4, 78.3) times increased risk of developing placenta previa respectively. Similarly, women with 2 or more previous abortions had a 2.1 (95% CI 1.2, 3.5) times increased risk of subsequently developing placenta previa. CONCLUSION: There is a strong association between previous cesarean section and risk of subsequent development of placenta previa. This risk increased with the number of previous cesarean sections. Increasing frequency of abortions was also found to predispose a woman to placenta previa.

Abortion, Induced↗
PubMed1997

Pharmacokinetics of oxcarbazepine and carbamazepine in human placenta.

PURPOSE: To study the transfer and metabolism of oxcarbazepine (OCBZ) and 10-hydroxy-10,11-dihydrocarbamazepine (10-OH-CBZ) and carbamazepine (CBZ) metabolism and its possible induction in human placenta. METHODS: A dual recirculating human placental perfusion system, blood sampling, high performance liquid chromatography (HPLC), reverse transcriptase-polymerase chain reaction (RT-PCR), and enzyme assays. RESULTS: OCBZ was metabolized into 10-OH-CBZ in five human placental cotyledons perfused for 2 h in a dual recirculating perfusion system. The same metabolite was found by HPLC in three sample pairs of maternal and cord blood taken during delivery from patients on OCBZ therapy. In all of the clinical samples, 10,11-trans-dihydroxy-10,11-dihydrocarbamazepine (10,11-D) was also found, but not in the perfusions. In addition, 10-OH-CBZ was not metabolized in the placental perfusions. The transfer of OCBZ through the perfused placentas was quicker than the transfer of antipyrine, while the transfer of 10-OH-CBZ was slower. Both OCBZ and 10-OH-CBZ also accumulated in placental tissue. CBZ metabolism was studied in three perfusions using placentas from mothers on CBZ therapy. No metabolism could be detected in the perfused placentas, while metabolites were found in both maternal and cord blood of the same mothers. Another series of placentas of mothers on CBZ therapy did not differ significantly from the placenta of a healthy mother as to CYP activities or the level of CYP3A4 mRNA. CONCLUSIONS: OCBZ is metabolized into 10-OH-CBZ to some extent in human placenta in vitro, suggesting that the placenta also participates in the metabolism of OCBZ in vivo. On the contrary, the placenta does not participate in the metabolism of CBZ. No induction of placental CBZ metabolism in vitro can be detected after maternal CBZ treatment during pregnancy.

Anticonvulsants↗
PubMed2005

Excretion of fetal biliverdin by the rat placenta-maternal liver tandem.

Fetal liver immaturity is accompanied by active heme catabolism. Thus fetal biliary pigments must be excreted toward the mother by the placenta. To investigate biliverdin handling by the placenta-maternal liver tandem, biliverdin-IXalpha was administered to 21-day pregnant rats through the jugular vein or the umbilical artery of an in situ perfused placenta. Jugular administration resulted in the secretion into maternal bile of both bilirubin and biliverdin (3:1). However, when biliverdin was administered to the placenta, most of it was transformed into bilirubin before being transferred to the maternal blood. Injecting Xenopus laevis oocytes with mRNA from rat liver or placenta enhanced their ability to take up biliverdin, which was inhibited by estradiol 17beta-d-glucuronide. The expression of three OATP isoforms in this system revealed that they have a varying degrees of ability to transport biliverdin (Oatp1/1a1 > Oatp2/1a4 > Oatp4/1b2). The abundance of their mRNA in rat trophoblast was Oatp1/1a1 >> Oatp4/1b2 > Oatp2/1a4. The expression of biliverdin-IXalpha reductase in rat placenta was detected by RT-PCR/sequencing and Western blot analysis. The relative abundance of biliverdin-IXalpha reductase mRNA (determined by real-time quantitative RT-PCR) was fetal liver > placenta > maternal liver. Common bile duct ligation in the last week of pregnancy induced an upregulation of biliverdin-IXalpha reductase in maternal liver but had no effect on fetal liver and placenta. In conclusion, several members of the OATP family may contribute to the uptake of fetal biliverdin by the rat placenta. Before being transferred to the mother, biliverdin is extensively converted into bilirubin by biliverdin-IXalpha reductase, whose expression is maintained even though bilirubin excretion into maternal bile is impaired.

Animals↗