Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PLACENTAL EXTRACTS”

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 1,207 records · Page 67Linked to original sources
PubMed1985

Relaxin concentrations in endometrial, placental, and ovarian tissues and in sera from ewes during middle and late pregnancy.

These studies were designed to determine the tissue source of ovine relaxin and to determine the feasibility of using the pregnant ewe for study of relaxin production and secretion. On Day 4 of gestation, ewes were laparotomized, the nonpregnant uterine horn was ligated, and the ovary not containing the corpus luteum was removed. During a second surgery at Day 45 (n = 8) or 140 (n = 9) of gestation, 10-ml blood samples were drawn from a uterine artery, the ovarian vein, and veins draining the pregnant and nonpregnant uterine horns. Endometrial, placental, and luteal tissues were obtained for immunocytochemistry and extraction. Relaxin was detected by a heterologous porcine radioimmunoassay (RIA) in 3 of 54 serum samples (701.3 +/- 25.4 pg/ml, mean +/- SEM). Relaxin was not detected in crude tissue extracts, but low quantities were detected by RIA following Sephadex G-50 column chromatography of tissue extracts. Total relaxin activity for all tissues was equivalent to 0.57 +/- 0.13 ng of porcine relaxin/g tissue (w.w.). Relaxin was not detected immunocytochemically by light or electron microscopy. These data indicate that low quantities of relaxin are present in tissues and sera of pregnant ewes.

Animals↗
PubMed2005

Human placental lipid induces melanogenesis through p38 MAPK in B16F10 mouse melanoma.

Melanogenesis is one of the characteristic functional activities of melanocyte/melanoma and is regulated via mitogen-activated protein kinase (MAPK) and Akt/protein kinase B (PKB) pathways. Placental total lipid fraction (PTLF), prepared from a hydroalcoholic extract of fresh term human placenta contains sphingolipids and was recently shown to stimulate melanogenesis via up-regulation of the key enzyme tyrosinase in B16F10 mouse melanoma cells. How such lipids mediate their effects on pigmentation and tyrosinase expression is a particularly important aspect of melanogenesis. To study the signaling that leads to tyrosinase expression, we have investigated the roles of the MAPK and Akt/PKB pathways in B16F10 melanoma cells in melanogenesis in response to PTLF. Treatment of cells with PTLF led to the time dependent phosphorylation of p38 MAPK. SB203580, a p38 MAPK inhibitor, completely blocked the PTLF-induced melanogenesis by inhibiting promoter activity and subsequent expression of tyrosinase. Phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002 a blocker of the Akt signaling pathway, or an inhibitor of MEK (MAPK/ERK Kinase), PD98059 when included along with PTLF was found to potentiate PTLF-induced phosphorylation of p38 MAPK together with tyrosinase expression and melanogenesis. The results suggest that the activation of p38 MAPK plays a crucial role in PTLF-induced B16F10 melanogenesis by up-regulating tyrosinase expression.

Animals↗
PubMed1991

In vitro mRNA degradation system to study the virion host shutoff function of herpes simplex virus.

The virion host shutoff (vhs) gene of herpes simplex virus encodes a virion polypeptide that induces degradation of host mRNAs at early times and rapid turnover of viral mRNAs throughout infection. To better investigate the vhs function, an in vitro mRNA degradation system was developed, consisting of cytoplasmic extracts from HeLa cells infected with wild-type herpes simplex virus type 1 or a mutant encoding a defective vhs polypeptide. Host and viral mRNAs were degraded rapidly in extracts from cells productively infected with wild-type herpes simplex virus type 1 but not in extracts from mock-infected cells or cells infected with the mutant vhs1. In contrast, 28S rRNA was stable in all three kinds of extract. Accelerated turnover of host mRNAs was also observed in extracts from cells infected with wild-type virus in the presence of dactinomycin, indicating that the activity was induced by a structural component of the infecting virions. The in vitro vhs activity was inactivated by heat or proteinase K digestion but was insensitive to brief treatment of the extracts with micrococcal nuclease. It was not inhibited by placental RNase inhibitor, it exhibited a strong dependence upon added Mg2+, it was active at concentrations of K+ up to 200 mM, and it did not require the components of an energy-generating system. In summary, the in vitro mRNA degradation system appears to accurately reproduce the vhs-mediated decay of host and viral mRNAs and should be useful for studies of the mechanism of vhs action.

Animals↗
PubMed1990

Alterations in transfer and lipid distribution of arachidonic acid in placentas of diabetic pregnancies.

Placental tissue from nondiabetic term pregnancies and pregnancies complicated by maternal insulin-dependent diabetes mellitus (IDDM) was perfused in vitro to compare the transfer and lipid distribution of arachidonic acid (AA). Radiolabeled albumin-bound AA was administered into the maternal afferent circulation, and samples of fetal and maternal effluent were collected at 10-min intervals. Perfused placental tissue was collected at the end of each experiment. The effluent was analyzed for total radioactivity, and extracts were subjected to thin-layer chromatography for the assessment of radioactivity associated with various lipid fractions. Placental AA uptake was significantly increased in perfused tissue from diabetic pregnancies (0.88 vs. 1.72 nM.min-1.g-1 in nondiabetic and IDDM, respectively; P less than 0.01), as was AA transfer (0.22 vs. 0.42 ml/min in nondiabetic and IDDM, respectively; P less than 0.01). However, transfer of the highly diffusible marker substance antipyrine was significantly reduced in IDDM placentas (1.79 vs. 2.49 ml/min in IDDM and nondiabetic, respectively; P less than 0.01). Compared with nondiabetic placentas, incorporation of AA into triglyceride was significantly increased in both maternal and fetal effluents and in placental tissue from IDDM pregnancies, whereas the percentage of AA remaining unesterified was reduced in both placental tissue and fetal effluent. Incorporation of AA into phosphoglycerides was significantly reduced in placental tissue but increased in fetal effluent in placentas from IDDM pregnancies. The results of these studies suggest that transfer and lipid distribution of AA are significantly altered in placentas from IDDM pregnancies. These findings may be relevant to the increased incidence of abnormal fetal growth and development associated with IDDM pregnancies.

Arachidonic Acids↗
PubMed1979

Isolation and tissue localization of type AB2 collagen from normal lung parenchyma.

Type AB2 collagen was isolated from normal lung parenchyma by pepsin extraction followed by differential salt extraction. This collagen comigrates with AB2 collagen isolated from placental membranes when run on 5% polyacrylamide gel electrophoresis; it has an alpha A and alpha B polypeptide chain ratio of 1 : 2 and a cyanogen bromide peptide profile similar to known AB2 collagen on 7.5% polyacrylamide gel electrophoresis. This AB2 collagen isolated from lung tissue specifically inhibits passive hemagglutination of affinity-purified rabbit antibodies to AB2 collagen isolated from amnionic and chorionic membranes. By indirect immunofluorescence microscopy, AB2 collagen was found to be widely distributed throughout the lung and was found preferentially associated with cell surfaces (basement lamina) and basement membranes.

Basement Membrane↗
PubMed1985

Human placental alkaline phosphatase in benign and malignant ovarian neoplasia.

In benign and malignant ovarian tumor patients, human placental alkaline phosphatase (HPLAP) was determined in serum and extracts from surgical tumor biopsies using a highly specific enzyme-antigen immunoassay based on a mouse monoclonal antibody (E6) to HPLAP. Serum HPLAP levels greater than or equal to 0.1 unit/liter were found in 58% of ovarian cancer patients. Serum carcinoembryonic antigen levels were positive (greater than 5.4 ng/ml) in 17% of these patients. HPLAP was detected in extracts from 13 of the 14 tumors investigated (range, 2.4 to 557 milliunits/g). Only the mixed heterologous Müllerian sarcoma was negative. The highest HPLAP content of normal ovarian tissue was 1.1 milliunits/g. The amount of heat-stable and L-p-bromotetramisole-insensitive alkaline phosphatase was in all cases much higher than the fraction recognized by E6. The neoplastic origin of HPLAP was confirmed immunohistochemically on paraffin sections by an indirect avidin-biotin-peroxidase staining procedure using E6. The staining pattern was compared to the histochemical distribution of total alkaline phosphatase on adjacent sections. A consistency was found between the amount of HPLAP in tissue extracts and its immunohistochemical distribution. In all the tumors, staining for HPLAP was observed mainly on the plasma membranes of carcinoma cells. In 9 of the 10 carcinomas, the histological distribution of HPLAP and also of total alkaline phosphatase was heterogeneous. HPLAP staining, present in one of five normal ovaries, was restricted to germinal inclusion cysts. The present results support the hypothesis that serous ovarian tumors originate from these cysts.

Alkaline Phosphatase↗
PubMed1993

[The conservative treatment of placenta accreta. A clinical case report].

The following description is a clinical case of placenta accreta and its conservative treatment. According to some authors, abnormal adhesion of the placenta depends on the alteration of the equilibrium between the trophoblastic tissue invasion and the reaction of the decidua. Consequently we have various degrees of penetration of the myometrium by chorionic villi into areas of deficit, sparse or absent decidua. Whatever the pathogenetic mechanism, the final clinical picture is slight to deep penetration of the trophoblastic tissue into the uterine wall. That causes absence of the normal plane of cleavage between placenta and maternal decidua, no spontaneous placental detachment during the third stage of labour and no possible manual removal. The patient, primigravida, was admitted at the 36th Week of gestation with PROM and physiologically delivered a neonate weighing 1820 g, after she spontaneously began labour. The newborn was admitted in the neonatal-pathology ward because it was premature although the Apgar score at 1-5 minutes after birth was 5-9. Placental ejection was awaited for 1 hour, then manual exploration of the uterine cavity was undertaken. The normal plane of cleavage between placental tissue and decidua was absent and therefore manual extraction of the placenta was impossible. Surgery was stopped and, after informed consensus was obtained from the patient, a conservative treatment was tried. After cutting the umbilical cord as short as possible and checking for vaginal bleeding, the patient was moved to obstetrics ward.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Determination of lamivudine in plasma, amniotic fluid, and rat tissues by liquid chromatography.

An HPLC method for the quantification of lamivudine (3TC) in rat plasma, amniotic fluid, placental and fetal tissues has been developed, validated and applied to the study of the placental transport of this drug in the pregnant rat. Placental and fetal tissues were processed using liquid-liquid extraction enhanced by salting out the sample using a saturated solution of ammonium sulfate. Plasma and amniotic fluid samples were processed by protein precipitation using 2 M perchloric acid. Reverse phase chromatography was performed using a phenyl column (5 microm, 150 mm x 2 mm i.d.) under a flow rate of 0.2 ml/min. The mobile phase consisted of 5% methanol in 20 mM dibasic phosphate buffer (pH 6). The method was validated over the range from 0.1 to 50 microg/ml for plasma and amniotic fluid and 0.2-50 microg/ml for the placental and fetal tissues.

Amniotic Fluid↗
PubMed1978

Placental-like alkaline phosphatase in malignant and benign ovarian tumors.

Alkaline phosphatase (ALP) components in extracts of seven malignant and eleven benign ovarian tumors were characterized using the criteria of electrophoretic mobility before and after neuraminidase treatment, heat stability, L-phenylalanine inhibition and reactivity against antiplacental ALP antiserum. Seven of the eighteen tumors had ALP components which most closely resembled the ALP isoenzyme normally found in placenta and were clearly distinguished from all other tissue ALPs. The proportion of tumors with the placental-like ALP in the malignant group (five out of seven) was significantly greater than the proportion in the benign group (two out of eleven). The fraction (78%) of the malignant tumors with the isozyme represents a larger percentage than has previously been found by examination of cancer patients' sera. The electrophoretic mobilities of the placental-like ALPs in the tumors were in no case identical to the mobilities of any of the six common placental ALP phenotypes. The tumor ALPs may thus be determined by rare variant alleles at the ALP locus, or alternatively, the enzyme molecules may have been subject to structural modification. At least two of these tumors contained an electrophoretically slow. heat-stable, leucine-sensitive ALP, which may correspond to what has been termed the D-variant of placental ALP found in some other tumors.

Adult↗
PubMed1986

Purification of human placental glucocerebrosidase using a two-step high-performance hydrophobic and gel permeation column chromatography method.

Glucocerebrosidase was purified from human placenta approximately 10,600-fold to apparent homogeneity with an overall yield of 37% using cholate extraction, ammonium sulfate fractionation, butanol delipidation, and a two-step high-performance hydrophobic and gel permeation column chromatography method. A Phenyl-5PW (21.5 X 150 mm) column was used in the first step. Approximately one litre of delipidated and dialysed extract containing 3.7 X 10(6) units of enzyme activity from 1 kg of placental tissue was processed by the column at a flow rate of 5 ml/min. Glucocerebrosidase was eluted using a linear cholate gradient (2-3%). There was a 50-fold purification and 89% recovery. The run was completed in about 7 h. In the second step, the concentrated enzyme preparation from the phenyl column was run through two Bio-Sil TSK 250 gel permeation columns (21.5 X 600 mm) connected in series at a flow rate of 1.5 ml/min. A symmetrical peak of glucocerebrosidase activity (Ve = 253 ml) which had constant specific activity (47,000 units/h/mg protein) was noted. There was a 17-fold purification and 80% recovery in this run which was completed in 4 h. Sodium dodecylsulfate-polyacrylamide gel electrophoresis and protein staining with silver compounds of the purified preparation revealed the presence of one band of Mr 68,000.

Chromatography, Gel↗
PubMedDate not supplied

Putative role of placental corticotropin-releasing factor in the mechanisms of human parturition.

Corticotropin-releasing factor is a 41-amino-acid neuropeptide synthesized in the paraventricular nucleus of the hypothalamus and released in response to stress. Its major role is the regulation of the hypothalamus-pituitary-adrenal axis by stimulation of ACTH release from the anterior pituitary gland. In addition, corticotropin-releasing factor modulates behavioral, vascular, and immune responses to stress. Corticotropin-releasing factor was first detected in the extracts of human placentas obtained at full term from spontaneous deliveries. Placental corticotropin-releasing factor content and messenger RNA expression progressively increase during normal pregnancy, and corticotropin-releasing factor levels in maternal plasma have a similar time course. The addition of corticotropin-releasing factor to primary trophoblast cell cultures stimulates ACTH secretion in a dose-dependent manner, and its action is mediated by cyclic adenosine monophosphate as second messenger. In addition, corticotropin-releasing factor is a potent local regulator of myometrial contractility and of membrane prostaglandin release. The effects of corticotropin-releasing factor in these various tissues are mediated by specific receptors. Placental corticotropin-releasing factor is also secreted into the fetal circulation and the stimulation of fetal pituitary ACTH and fetal adrenal gland dehydroepiandrosterone sulfate release in vitro has been shown. Recently, urocortin, a new peptide related to corticotropin-releasing factor, has been found in human placenta. Corticotropin-releasing factor and urocortin share some of their biologic effects, acting on the same receptors. A large-molecular-weight corticotropin-releasing factor-binding protein modulates the activity of both these peptides. Plasma corticotropin-releasing factor levels are low in nonpregnant women and become higher during the second trimester of pregnancy, rising steadily until about 35 weeks, and then increasing more rapidly until term. Vaginal delivery is a condition associated with the highest values of maternal corticotropin-releasing factor levels. Corticotropin-releasing factor is also measurable in fetal plasma (20-fold lower than in maternal circulation) and in amniotic fluid. Increased maternal plasma corticotropin-releasing factor levels characterize some gestational diseases. Women with chronic hypertension and preeclampsia have high corticotropin-releasing factor levels, and intrauterine growth retardation is associated with an activation of the hypothalamus-pituitary-adrenal axis, reflected by increased fetal plasma concentrations of ACTH, cortisol, and corticotropin-releasing factor. The role of corticotropin-releasing factor in preterm labor is uncertain, but midgestational plasma corticotropin-releasing factor levels may be higher in women delivering preterm. In these various pathologic states, maternal plasma corticotropin-releasing factor-binding protein levels undergo opposite changes, decreasing to very low levels. The endocrine-paracrine corticotropin-releasing factor/corticotropin-releasing factor-binding protein pathways may play a major role in the mechanism of human parturition.

Carrier Proteins↗
PubMed2001

Placental nitric oxide synthase (NOS) activity and nitric oxide (NO) production in normal pregnancy, pre-eclampsia and eclampsia.

OBJECTIVES: To measure nitric oxide synthase (NOS) activity and total nitrites levels (as an index of nitric oxide 'NO' production) in placental villous homogenate of normal, pre-eclamptic and eclamptic pregnant women. DESIGN: Two groups were studied cross-sectionally: late pregnant women with pre-eclampsia and eclampsia (n=31) and normal pregnant women (all late) as controls (n=32). Two tissue blocks of whole placenta, each 1 x 1 x 1 cm, were collected at delivery and assayed for NOS activity and total nitrite levels. SETTING: Department of Obstetrics and Gynecology, Assiut University Hospitals, Egypt. METHODS: Placental tissues were homogenized and villous homogenates were assayed for NO production by Griess reaction which measures the combined oxidation products for NO (nitrites and nitrates) after reduction with nitrate reductase. NOS activity was determined by measuring NO synthesis by tissue extracts spectrophotometrically using the oxidation of oxyhemoglobin to methemoglobin by NO. RESULTS: Placental villous homogenates of pregnancies complicated by pre-eclampsia and eclampsia had significantly higher NOS activity and total nitrites levels compared with those of normal pregnancy [for NOS (P<0.0001) and for total nitrites (P<0.001)]. CONCLUSIONS: (1) Placental NOS activity and NO production are significantly increased in pre-eclampsia and eclampsia than those of normal pregnancy; this increase was directly related to the severity of this disorder. (2) Such increase possibly represents a physiologic adaptive response to overcome the increased placental vascular resistance and to minimize platelet and leukocyte adhesion to the surface of placental villi or within the intervillous spaces.

Adult↗
PubMed2002

Naloxone for narcotic-exposed newborn infants.

BACKGROUND: Naloxone, a specific opiate antagonist, is available for the management of newborn infants with respiratory depression that may be due to transplacentally-acquired opiates. However, it is unclear which groups of newborn infants may benefit from this therapy, and whether naloxone has any harmful effects. OBJECTIVES: In newborn infants who have been exposed trans-placentally to narcotics, does naloxone reduce the need for, or duration of, ventilatory support or neonatal unit admission. SEARCH STRATEGY: The standard search strategy of the Cochrane Neonatal Review Group was used. This included electronic searches of the Cochrane Controlled Trials Register (The Cochrane Library, Issue 1, 2002), MEDLINE (1966 - February 2002), EMBASE (1988 - February 2002), and previous reviews including cross references. SELECTION CRITERIA: Randomised controlled trials comparing the administration of naloxone versus placebo, or no drug, or another dose of naloxone, to newborn infants with suspected or confirmed trans-placental exposure to narcotics. DATA COLLECTION AND ANALYSIS: Data were extracted using the standard methods of the Cochrane Neonatal Review Group, with separate evaluation of trial quality and data extraction by each author and synthesis of data using relative risk, risk difference and weighted mean difference. MAIN RESULTS: We found nine trials that compared the effects of naloxone versus placebo or no drug in newborn infants exposed to maternal narcotic analgesia prior to delivery. The main outcomes reported were measures of respiratory function in the first six hours of life. Although we found some evidence that naloxone increases alveolar ventilation, we did not find any data on the pre-specified primary outcomes of this review: the need for assisted mechanical ventilation or admission to a neonatal unit. REVIEWER'S CONCLUSIONS: There is a need for a randomised controlled trial to determine if naloxone confers any clinically important benefits to newborn infants with respiratory depression that may be due to trans-placentally acquired narcotic.

Female↗
PubMed1987

Identification of dynorphin 1-8 in human placenta by mass spectrometry.

The human placental villus tissue contains opioid receptors and peptides. The opioid peptides extracted from the villus tissue were fractionated using reverse-phase high performance liquid chromatography and a radio-receptor assay. The presence of dynorphin 1-8 was corroborated by mass spectrometric production of (M + H) ion in the fast atom bombardment mode. This octa-peptide could be the natural ligand of the kappa opioid receptors present in the human placental villus tissue.

Chorionic Villi↗
PubMed1988

Sex hormones modulate the synthesis of basic fibroblast growth factor in human endometrial adenocarcinoma cells: implications for the neovascularization of normal and neoplastic endometrium.

Basic fibroblast growth factor (bFGF) has been demonstrated to exert an angiogenic activity in vivo. Here, the ability of bFGF to stimulate plasminogen activator (PA) production in bovine capillary endothelial cells was used as an assay for the presence of bFGF-like molecules in the extracts of the human endometrial adenocarcinoma AN3CA, HEC-1-A, and HEC-1-B cell lines. The identity of the PA-stimulating activity with bFGF was confirmed by its high affinity for heparin and by its cross-reactivity with antibodies to human placental bFGF. Western blot analysis and immunoprecipitation experiments showed that, in the extracts of the three cell lines, these antibodies recognize a protein with an apparent molecular weight of approximately 17,000 daltons. 17 beta-Estradiol stimulates the synthesis of this bFGF-like molecule in all the endometrial cell lines tested. This stimulation can be abolished by treating the cells with progesterone. These data demonstrate the capacity of sex hormones to regulate bFGF synthesis in tumor endometrial cells, and they suggest that bFGF may play a role in the vascularization of the endometrial adenocarcinoma as well as of the normal endometrium.

Adenocarcinoma↗
PubMed1997

The effect of placental removal method on the incidence of postcesarean infections.

OBJECTIVE: Our purpose was to determine whether the incidence of postoperative endometritis and wound infection is associated with the method of placental removal at the time of cesarean section. STUDY DESIGN: Parturients undergoing cesarean delivery were prospectively randomized to have the placenta removed manually or spontaneously. Patients were excluded from participation if they had received intrapartum prophylactic antibiotics or had been determined to have chorioamnionitis. After delivery of the infant women in the manual group had the placenta extracted by the primary surgeon, whereas women in the spontaneous group had the placenta delivered by gentle traction on the umbilical cord. All study subjects received perioperative prophylactic antibiotics. The primary outcome variable was a postcesarean infection, defined as postecsarean endometritis or wound cellulitis requiring drainage and antibiotic therapy. RESULTS: A total of 333 women were enrolled in the investigation, with 165 assigned to the manual removal group and 168 allocated to have spontaneous removal. There were no statistically significant differences in mean gestational age, frequency or duration of ruptured membranes, frequency or duration of labor, or mean number of vaginal examinations between the two study groups. Postoperative infections occurred in 25 of 168 (15%) women in the spontaneous delivery group compared with 44 of 165 (27%) women in which the placenta was manually extracted (relative risk 0.6, 95% confidence interval 0.4 to 0.9, p = 0.01). Subset analysis of patients delivered with ruptured membranes similarly demonstrated a statistically significant reduction in the incidence of postoperative infections with spontaneous placental removal compared with manual extraction (20% vs. 38%, relative risk 0.5, 95% confidence interval 0.3 to 0.9, p = 0.02). There was a similar trend toward a reduction in postdelivery infections associated with spontaneous placental removal in women with intact membranes; however, this difference did not attain statistical significance. CONCLUSIONS: Spontaneous delivery of the placenta after cesarean delivery is associated with a decrease in the incidence of postcesarean infections.

Cesarean Section↗
PubMed1988

Methylated DNA-binding protein is present in various mammalian cell types.

A DNA-binding protein from human placenta, methylated DNA-binding protein (MDBP), binds to certain DNA sequences only when they contain 5-methylcytosine (m5C) residues at specific positions. We found a very similar DNA-binding activity in nuclear extracts of rat tissues, calf thymus, human embryonal carcinoma cells, HeLa cells, and mouse LTK cells. Like human placental MDBP, the analogous DNA-binding proteins from the above mammalian cell lines formed a number of different low-electrophoretic-mobility complexes with a 14-bp MDBP-specific oligonucleotide duplex. All of these complexes exhibited the same DNA methylation specificity and DNA sequence specificity. From the extracts of rat and calf tissues, oligonucleotide protein complexes formed that also had the same specificity as human placental MDBP although they had a higher electrophoretic mobility probably due to digestion by proteases in the nuclear extracts. Although MDBP activity was found in various mammalian cell types, it was not detected in extracts of cultured mosquito cells and so may be associated only with cells with vertebrate-type DNA methylation.

5-Methylcytosine↗
PubMed2004

Functional assessment of ABCG2 (BCRP) gene polymorphisms to protein expression in human placenta.

The aim of the present study was to assess the contribution of polymorphisms in the breast cancer resistance protein/ATP-binding cassette transporter G2 (BCRP/ABCG2) gene to the placental expression from a new perspective, allelic imbalance. Polymorphisms were screened by polymerase chain reaction (PCR)-single-strand conformation polymorphism analysis followed by sequencing with DNA extracted from 100 placentas. To examine whether polymorphisms of the BCRP gene correlate with the placental BCRP expression, we determined mRNA and protein levels by quantitative real-time PCR and Western blotting, respectively. In placentas, G34A (Val(12)Met) and C421A (Gln(141)Lys) were frequently observed (18-36%), but C376T, which creates a stop codon (Gln(126) stop codon), was found with an allelic frequency of 1%. The mean of the BCRP protein level was significantly lower (p < 0.05) in homozygotes for the A421 allele than in those for the C421 allele, and heterozygotes had an intermediate value. To evaluate whether the C421A polymorphism acts as a cis-element in BCRP transcription, allelic imbalance was determined using informative lymphoblasts and 56 samples of placental cDNA. In most of the placental samples we tested, the difference in expression levels between the two alleles was small, and only two samples indicated a monoallelic expression (i.e., preferential expression of one allele). These results suggest that 1) the predominant allelic expression pattern of BCRP in placental samples is biallelic, and 2) the mutation C421A is not a genetic variant acting in cis, but is considered to influence the translation efficiency.

ATP Binding Cassette Transporter, Subfamily G, Mem↗