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PubMed1997

The demonstration of progesterone, but not of estrogen, receptors in the developing human placenta.

Since presence of steroid receptors in the human placenta has been the subject of dispute, we have investigated the existence of estrogen (ER) and progesterone (PR) receptors in trophoblasts across gestational age by a variety of different techniques. Fresh human placental tissue of trimesters 1 to 3 was paraffin-embedded or snap-frozen (-80 degrees C) and sliced (5 microns). Other tissue fragments from identical placentae were dispersed and incubated in monolayer cultures for up to 5 days. Immunocytochemistry (ICC) was performed for ER and PR in both trophoblast cells in culture and in whole tissue slices, using the sandwich antibody technique with subsequent horse-radish peroxidase reaction for colorization. In addition, long-term perifusion studies were conducted with explants of term placentae, using perifusion medium with estradiol (E, 2 ng/ml) and/or progesterone (P, 200 ng/ml). Perifused explants were then subjected to further ICC staining. Furthermore, RT-PCR for both ER and PR mRNA was performed for detection of the gene products in placentae of different gestational ages. Lastly, binding studies with iodine or tritium-labeled E and P were conducted on cytosol fractions. In placental sections and cultured trophoblasts, PR was clearly demonstrable in all placentae across different gestational ages. Abundant PR signal was found adjacent to the nuclei, and additionally in the dendrite-like pseudopods of syncytiotrophoblast cells. In contrast, no such staining signal was detected for the ER; this finding applied under all conditions investigated and at all gestational ages. Again, no staining for ER by ICC was detected in any tissue after perifusion with sex steroids. RT-PCR revealed no product for ER, but only for PR, in placentae across all gestational ages. Binding studies with labeled E and P showed no binding for either compound. Taken together, these observations suggest the presence of PR, but not of ER, in human placenta throughout gestation. Our failure to detect the ER does not entirely preclude the presence of this receptor in human trophoblasts, but might be attributed to a relatively low number and density of ER on these cells. Alternatively, estrogen's action on the placenta may be mediated by a different type of ER, such as by a non-classical membrane-bound receptor.

Binding Sites↗
PubMed2001

Low maternal serum levels of placenta growth factor as an antecedent of clinical preeclampsia.

OBJECTIVE: Maternal serum placenta growth factor levels have been shown to be significantly reduced in women with established preeclampsia. However, the temporal change in serum placenta growth factor levels before the clinical onset of preeclampsia is not known. STUDY DESIGN: Serum samples were collected from patients at the first prenatal (5-15 weeks' gestation), second-trimester (16-20 weeks' gestation), and third-trimester (26-30 weeks' gestation) visits. Serum placenta growth factor levels were determined and analyzed according to pregnancy outcome. RESULTS: Maternal placenta growth factor levels during normal gestation increased dramatically from the first to the third trimester. At the same gestational time points, in contrast, significantly lower serum placenta growth factor levels were found in patients in whom mild or severe preeclampsia eventually developed (P <.01). Low maternal serum placenta growth factor levels during early gestation were associated with a significant odds ratio for development of preeclampsia (P <.005). CONCLUSION: Relatively decreased levels of serum placenta growth factor occur before the onset of clinical preeclampsia, which suggests that placenta growth factor measurement could be used to discriminate those pregnancies predisposed to development of preeclampsia.

Adult↗
PubMed2001

Placenta growth factor is not an early marker for the development of severe preeclampsia.

OBJECTIVE: Our purpose was to determine whether plasma concentrations of placenta growth factor may be used as a marker for women who ultimately have severe preeclampsia. STUDY DESIGN: We performed a nested case-control study to compare plasma concentrations of placenta growth factor in women with severe preeclampsia with the concentrations in normotensive pregnant control subjects. Plasma samples were collected at <20 weeks' gestation and again in the third trimester. Twenty-two women who ultimately had severe preeclampsia were matched for gestational age at delivery with 22 normotensive control subjects. Placenta growth factor concentrations were measured by a specific antigen capture enzyme-linked immunosorbent assay. Comparisons were made by using the Mann-Whitney U test for nonparametric data such as placenta growth factor concentrations. The Student t test was used for parametric data. RESULTS: A total of 880 pregnant women were screened. Severe preeclampsia developed in 22, for an incidence of 2.5%. As expected, women with severe preeclampsia had significantly higher systolic and diastolic blood pressures, and their infants had lower birth weights. Placental weights at delivery were similar between those with severe preeclampsia and control subjects (659 vs 699 g; P =.51). During the third trimester, the median placenta growth factor concentrations were significantly lower in women with severe preeclampsia than in normotensive control subjects (125 vs 449 pg/mL; P =.003). When samples drawn at <20 weeks' gestation were compared, there was no difference between the group with severe preeclampsia and those who remained normotensive (98.8 vs 56.34 pg/mL; P =.15). CONCLUSION: During the third trimester, patients with severe preeclampsia have decreased maternal concentrations of placenta growth factor. This difference is not seen earlier in pregnancy. Lower concentrations of placenta growth factor may be a result of severe preeclampsia rather than a causal factor. Placenta growth factor is not a good marker for the subsequent development of severe preeclampsia.

Biomarkers↗
PubMed2001

HIV-1 in placentas of untreated HIV-1-infected women in relation to viral transmission, infectious HIV-1 and RNA load in plasma.

The presence of HIV in the placenta was analysed in relation to virological and immunological factors and vertical transmission of HIV in 39 pregnancies between 1989 and 1993 among 37 HIV-1-infected women without zidovudine prophylaxis. HIV-1 was detected in 12 of 37 (31%) placentas by immunohistochemistry and in 3 of 18 by PCR. Altogether 14/39 (36%) placentas bore evidence of HIV-1 infection, although there was no relation with the outcome of HIV infection in the child. Neither was there a relation between placental infection and either CD4 cell counts or HIV-1 RNA levels. However, HIV-1 was isolated from plasma in 20 of 39 (50%) pregnancies, which was inversely related to the presence of HIV in the placenta. When HIV-1 was identified in the placenta, HIV-1 was isolated from plasma in 3/14 (21%) pregnancies, vs 17/25 (68%) when it was not (p = 0.01), with a relative risk of having a placenta positive for HIV of 3.9 in pregnancies with a negative plasma HIV isolation. This inverse relation may point to differences in tropism between HIV-1 in placenta and plasma. The results show that the placental barrier prevents HIV transmission, irrespective of whether HIV enters the placenta or not.

CD4 Lymphocyte Count↗
PubMed1987

Differential expression of MHC class I antigens on the placenta of the rat. A mechanism for the survival of the fetal allograft.

In some mating combinations in rats, there is a maternal antibody response to the maternal antigenic components of the placenta without any previous immunization of the mother. The highest response occurs in the WF (u) female mated to the DA (a) male, and it is against a unique MHC-encoded class I antigen, the Pa antigen, and not against the major allele-specific transplantation antigen of the DA strain, RT1.Aa. The development of mAbs to the Pa and Aa antigens allowed us to localize these antigens on the placenta and to explore the reason for the differential antibody response to them using immunohistochemical and biochemical techniques. Both antibodies reacted with the WF X DA placenta and stained the endovascular and interstitial trophoblast of the decidua, the basal trophoblast, Reichert's membrane, and the yolk sac epithelium, but they did not stain the labyrinthine trophoblast. Blocking studies showed that each antibody reacted with a separate molecule in the placenta. Anti-class II mAbs reactive with the a or u haplotype did not stain the WF X DA, DA X DA, or WF X WF placenta; hence, there are no class II antigens in the placenta. Electron microscopic studies of the semiallogeneic WF X DA placenta using the immunogold technique with both single- and double-labeling showed that only the Pa antigen was expressed on the surface of the basal trophoblast, but that both the Pa and Aa antigens were in the cytoplasm of these cells; neither antigen was found in the labyrinthine trophoblast. By contrast, the placenta from the syngeneic DA X DA mating expressed both the Pa and Aa antigens on the surface of the basal trophoblast as well as in the cytoplasm; neither antigen was found in the labyrinthine trophoblast. These observations were quantified morphometrically using electron photomicrographs of single-labeled tissues. Both the Pa and Aa antigens isolated from the plasma membrane of lymphocytes have heavy chains of 46 kD, but those antigens isolated from the plasma membrane of basal trophoblast cells have heavy chains of 43 kD. Based on densitometric measurements of autoradiographs, the Pa/Aa ratio in the basal trophoblast membrane is 23.5, whereas it is 0.46 in lymphocyte membranes. These studies show that there is differential regulation of the expression of class I antigens on basal trophoblast cells in semiallogeneic pregnancies, but not in syngeneic pregnancies, such that the major allele-specific transplantation antigen is scarcely expressed on the surface of the basal trophoblast.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Subchorionic fibrin cultures for bacteriologic study of the placenta.

Previous bacteriologic studies of the placenta have been hampered by a high rate of contamination of vaginal flora. In the present study, cultures of the subchorionic fibrin layer of the placenta were compared to conventional swab-cultures of the surface of the fetal membranes for recovery of aerobic and anaerobic bacteria. Parallel cultures of membrane surface and subchorionic fibrin (SCF) were done in the placentas of 33 deliveries suspected clinically of being complicated by infection (CD). Placentas from 46 uncomplicated deliveries were similarly cultured to serve as controls. SCF cultures were positive in 11 of 33 CD placentas and in only 1 of 46 controls (P less than 0.001). SCF cultures showed contaminating vaginal flora in 2 of 79 while surface cultures showed vaginal contamination in 16 of 79 (P less than 0.01). Recovery of pathogens was similar by the two methods: 10 of 33 and 14 of 33 respectively. One hundred ninety-one additional CD placentas were cultured by the SCF technique. Forty-nine of the 224 SCF cultures yielded pathogens with a predominance of group B hemolytic streptococci, anaerobic gram positive cocci and anaerobic gram negative rods (81 total isolates). Escherichia coli was isolated in 5 cases. Cultures showing exclusively contaminating vaginal flora were obtained from only 3 of the 224 placentas. Subchorionic fibrin cultures combine technical simplicity, low rate of contamination and excellent recovery of pathogens. The bacterial types found by this method are the predominant species that cause endometritis, pelvic infections, and neonatal septicemia. Subchorionic fibrin culture is a useful technique for the bacteriologic diagnosis of infection in the placenta.

Bacteria↗
PubMed2001

Expression of insulin-like growth factor-I and placental growth hormone mRNA in placentae: a comparison between normal and intrauterine growth retardation pregnancies.

Intrauterine growth restriction (IUGR) is generally defined as the pathological restriction of fetal growth resulting in a fetus with birth weight below the 10th percentile for gestational age. Almost 75% of IUGR cases develop during third trimester. Studies on animals (rodents and sheep) as well as humans suggest that insulin-like growth factor-I (IGF-I), under the influence of placental growth hormone (PGH) plays crucial roles in fetal growth regulation during this period. Limited data are available with regard to IGF-I and PGH in placentae of normal and IUGR births. Therefore, in the present study, IGF-I and PGH mRNA expression has been studied in term placentae of normal (n = 10) and IUGR (n = 15) births by in-situ hybridization procedure. Their expression was also studied in first (n = 5) and second (n = 5) trimester placentae obtained from elective termination of normal pregnancies. Both IGF-I and PGH expression were found to be higher in the first and second trimester placentae compared to term placentae in normal pregnancies. However, IUGR term placentae showed increased expression of both IGF-I and PGH mRNA in comparison with normal placentae. Various mechanisms leading to the increased transcription of IGF-I and PGH mRNA in IUGR placenta are discussed. This increased transcription perhaps occurs in response to the reduction in the fetal growth.

Female↗
PubMed1999

Placenta previa: preponderance of male sex at birth.

To determine the relation between placenta previa and male sex at birth, the authors conducted two types of analysis: 1) a historical cohort analysis of singleton live births in New Jersey hospitals during 1989-1992 (N = 447,963); and 2) a meta-analysis of previously published studies on the subject. For the cohort analysis, subject mother-infant dyads were identified from linked birth certificate and maternal and infant hospital claims data. The infant's sex for mothers with an International Classification of Diseases, Ninth Revision, Clinical Modification, code of 641.0-641.1 for placenta previa (n = 2,685) was compared with infant's sex for mothers without placenta previa (n = 445,270). For the meta-analysis, seven published articles were located and summary effects were calculated using both fixed-effect and random-effects models. In the present cohort study, the male:female ratio at birth was significantly higher in women with placenta previa (1.19) than in those without placenta previa (1.05) (p<0.001). The association of placenta previa with male sex persisted when the analysis was either stratified or adjusted for the effects of maternal age, maternal parity, maternal smoking during the index pregnancy, race/ethnicity, the infant's gestational age, and the infant's birth weight. The meta-analytic results from the fixed-effect and random-effects models showed a 14% excess of placenta previa when women were carrying a viable male fetus as compared with a viable female fetus during pregnancy. The results were the same regardless of whether the present cohort study was included in the meta-analysis. In conclusion, the evidence obtained from these analyses strongly argues for an association between placenta previa and male sex at birth. The mechanism for this association remains to be determined.

Cohort Studies↗
PubMed2007

Pathologic examination of the placenta and observed practice.

OBJECTIVE: To estimate the percentage of deliveries eligible for pathologic examination of the placenta and compare with observed practice using the College of American Pathologists' (CAP) 1997 guidelines for examination of the placenta. METHODS: Records were reviewed from all live-birth deliveries 20 weeks or more of gestation in 2001 at Strong Memorial Hospital. The expected number of deliveries with CAP recommended indications was determined and compared with the observed number of deliveries in which the placenta was actually examined. Descriptive statistics, independent t tests, chi(2) tests, difference between two population proportions test, odds ratios, 95% confidence intervals, and multiple logistic regression were used to analyze the data. RESULTS: The observed number and percentage of deliveries with CAP recommended indications that had pathologic placental examination, 575 and 18.2% (95% confidence interval 16.9-19.6), was significantly lower (P<.001) than expected, 1,185 and 37.5% (95% confidence interval 35.8-39.2). The placenta was examined less frequently than expected in 9 of 14 categories. Independent predictors of examination of the placenta were gross placental abnormalities, multiple gestation, prematurity, peripartum fever, neonatal intensive care unit care of infant, cesarean delivery, and delivery by a maternal-fetal medicine specialist. CONCLUSION: Using the CAP guidelines for submission of the placenta would result in pathologic examination in 37.5% of all deliveries. Less than one half of all deliveries in which the placenta was eligible for submission were actually examined. Current advances in our understanding of pathologic conditions of the placenta and their relation to infant outcomes may warrant re-evaluating policy on placental examination at institutional and national levels. LEVEL OF EVIDENCE: II.

Adult↗
PubMed1992

Blood levels of prostaglandin metabolites (PGFM, PGEM) after parturition in cows with and without retained placenta considering spontaneous calving and dystocia.

Blood samples were taken from 71 Holstein Friesian cows at 0, 3, 24 and 48 hours after parturition. Peripheral plasma concentrations of prostaglandin F2 alpha and E2 metabolites (PGFM, PGEM) were determined by radioimmunoassay. The cows were divided into 4 groups, according to type of calving (spontaneous, dystocia) and discharge of placenta. Group 1: spontaneous calving, shedding of placenta within 12 hours (SC, NRP, n = 19); group 2: spontaneous calving, retained placenta (SC, RP, n = 7); group 3: Dystocia, shedding of placenta within 12 hours (Dys, NRP, n = 32); group 4: Dystocia, retained placenta (Dys, RP, n = 13). The PGFM concentrations decreased within 3 hours after parturition only in NRP cows (groups 1 and 3, p < 0.05). Three hours after calving the animals of group 3 had considerably higher PGFM levels than those in group 4 (0.46 +/- 0.26 vs 0.26 +/- 0.11 ng/ml). Significant decreases (p < 0.05) in PGEM concentrations occurred in cows that shed the placenta within 24 hours after parturition. Cows that retained the placenta showed a significant slower decrease of the PGEM levels. It is concluded that postpartum prostaglandin levels are influenced by stress during parturition (dystocia, transportation) as well as by retained placenta.

Animals↗
PubMed1996

Gestational changes in nitric oxide synthase activity in the rat placenta.

OBJECTIVE: To assess the importance of nitric oxide (NO) generated in the placenta on pregnancy, nitric oxide synthase (NOS) activities were measured in the rat placentas of different gestational ages. MATERIALS AND METHODS: NOS activity was determined by [3H] L-arginine to [3H]-citrulline conversion assay on rat placenta of day 5, 10, 15 and 21 of gestation. RESULTS: NOS activity distributed both in the soluble and particulate fractions. Inhibition of NOS activity by L-arginine analogs confirmed the substrate specificity. The requirement of calcium/calmodulin for the maximal activity indicated that the rat placenta NOS was of a constitutive calcium/calmodulin dependent isoform. The activities in both fractions were higher in the earlier gestational age placentas, decreasing with progression of gestation, and the lowest in the term placentas. CONCLUSION: Although NOS activity was detected in the placenta throughout gestation, it was highest in the early gestational age placenta, suggesting a possible significant role of NO in early gestation.

Animals↗
PubMed2001

Birthweight in liveborn twins: the influence of the umbilical cord insertion and fusion of placentas.

OBJECTIVE: To assess the relation of umbilical cord insertion and fusion of placentas with birthweight in monozygotic monochorionic, monozygotic dichorionic, and dizygotic twins. DESIGN: A prospective population study. POPULATION: 4529 liveborn twin pairs whose birthweight was recorded, placentas were examined, and site of umbilical cord insertion was determined after delivery. RESULTS: Infants with a peripheral cord insertion weighed 150g less (P < 0.001) than infants with a central cord insertion. Dizygotic infants had a significantly (P < 0.001) higher incidence of central cord insertion (82%) than monozygotic dichorionic (65%) and monozygotic monochorionic (53%) infants. Monozygotic dichorionic infants with fused placentas and a peripheral cord insertion weighed on average 300g less (P < 0.01) than infants with separate placentas and a central cord insertion. In dizygotic infants, fusion of the placentas did not affect birthweight. CONCLUSIONS: Umbilical cord insertion is associated with birthweight in all types of twins. Fusion of the placentas only affects the birthweight of monozygotic dichorionic, not that of dizygotic infants. This might be due to the greater proximity of implantation of monozygotic dichorionic twins. Dizygotic twins weighed more than monozygotic twins only when placentas were fused and cord insertion was peripheral. Hence, the difference between the mean birthweights of dizygotic, monozygotic dichorionic, and monozygotic monochorionic infants may originate from the least favourable antenatal situation, namely fused placentas with a peripheral cord insertion, which occurs most frequently in monozygotic twins.

Analysis of Variance↗
PubMedDate not supplied

Alcohol-metabolizing enzymes in placenta and fetal liver: effect of chronic ethanol intake.

Alcohol dehydrogenase and different subcellular distribution of aldehyde dehydrogenase (ALDH) in fetal liver and placenta at 15 and 21 days of gestation were studied in three different groups of pregnant rats: alcoholic, pair-fed, and rat solid chow diet animals. Chronic ethanol intake during pregnancy produced a decrease in fetal body and liver weight but an increase of placenta weight. No alcohol dehydrogenase was detected in placenta at any stage of gestation, nor in fetal liver at 15 days although a low activity was found at 21 days. No significant difference was observed from fetuses of alcoholic and nonalcoholic mothers. Subcellular aldehyde dehydrogenase distribution in placenta was similar to that in adult liver. Although no cytosolic ALDH was detected in fetal liver at any period of gestation, low activities were found in placenta and fetal liver at 15 days of pregnancy in other subcellular fractions. However, at 21 days the placental activity decreased while that of fetal liver increased markedly. The increase of the fetal liver ALDH was especially noticeable in the mitochondrial fraction in which the activity was approximately 10-fold higher than in the placenta mitochondrial fraction. A small decrease in placenta and fetal liver ALDH was observed in alcoholic rats. The role of the placenta ALDH in the acetaldehyde placental transfer is discussed.

Alcohol Oxidoreductases↗
PubMed1999

Histologic distribution and biochemical properties of alpha 1-microglobulin in human placenta.

PROBLEM: The embryo is protected from immunologic rejection by the mother, possibly accomplished by immunosuppressive molecules located in the placenta. We investigated the distribution and biochemical properties in placenta of the immunosuppressive plasma protein alpha 1-microglobulin. METHOD OF STUDY: Placental alpha 1-microglobulin was investigated by immunohistochemistry and, after extraction, by electrophoresis, immunoblotting and radioimmunoassay. RESULTS: alpha 1-Microglobulin staining was observed in the intervillous fibrin and in syncytiotrophoblasts, especially at sites with syncytial injury. Strongly stained single cells in the intervillous spaces and variably stained intravillous histiocytes were noted. Solubilization of the placenta-matrix fraction and placenta membrane fraction released predominantly the free form of alpha 1-microglobulin, but, additionally, an apparently truncated form from the placenta-membrane fraction. The soluble fraction of placenta contained two novel alpha 1-microglobulin complexes. CONCLUSIONS: The biochemical analysis indicates the presence in placenta of alpha 1-microglobulin forms not found in blood. The histochemical analysis supports the possibility that alpha 1-microglobulin may function as a local immunoregulator in the placenta.

Electrophoresis, Polyacrylamide Gel↗
PubMed2005

Tumor necrosis factor-alpha in the placenta is not elevated in pre-eclamptic patients despite its elevation in peripheral blood.

PROBLEM: Tumor necrosis factor-alpha (TNF-alpha) is present in human placental and uterine cells at the early and late stages of gestation and promotes the regulation of trophoblast growth and invasion. We evaluated whether TNF-alpha levels in the placenta and blood of pre-eclamptic women differed from those with normal pregnancies. METHOD OF STUDY: The subjects were 39 pregnant women carrying single fetuses (21 normal-pregnant and 18 pre-eclamptic patients). Their average gestational age at entry was 38-39 weeks. Peripheral blood was collected before the onset of labor and separated serum was stored at -20 degrees C. A tissue segment of the placenta was cut and frozen in liquid nitrogen immediately after delivery at -80 degrees C. The frozen placental tissue was added to phosphate-buffered saline. The tissue was fully homogenized and centrifuged. Separated supernatant was stored at -80 degrees C. TNF-alpha levels in separated serum and TNF-alpha and total protein (TP) levels in separated supernatant were measured. The presence of TNF-alpha in the placenta was evaluated by immunohistochemistry in five pre-eclamptic and five normal-pregnant patients. RESULTS: Serum TNF-alpha levels were higher in pre-eclampsia than in normal pregnancies. However, TNF-alpha/TP levels in the placenta did not differ significantly between the two groups. As for TNF-alpha immunostaining of trophoblastic cells in the placenta, it was weak in three and moderate in two of the normal pregnancies, while it was absent in two, weak in one, and moderate in two in the pre-eclampsia group. CONCLUSIONS: We demonstrated no significant increase in TNF-alpha/TP levels in the placenta in pre-eclampsia despite a significant increase in serum TNF-alpha levels. There was no strong immunostaining for TNF-alpha detected by immunohistochemistry in the pre-eclampsia group. These findings suggest that TNF-alpha in the placenta is not a key cytokine to interfere with normal trophoblast invasion into the myometrium in pre-eclampsia, and that sources other than the placenta may contribute to the elevated levels of TNF-alpha found in the circulation of pre-eclamptic patients.

Adult↗
PubMed2005

Experimental genital mycoplasmosis causes increased levels of mRNA for IL-6 and TNF-alpha in the placenta.

PROBLEM: Previous studies with animal models have shown that injection of lipopolysaccharide (LPS) results in fetal loss and increases production of proinflammatory cytokines at the maternal-fetal interface. Most intrauterine infections, however, are associated with Ureaplasma urealyticum, a microorganism that lacks a cell wall and therefore does not contain LPS. Previous work in our laboratory with an animal model for genital infection with a similar organism, Mycoplasma pulmonis, revealed that widespread infection in maternal and fetal tissues can be experimentally induced with minimal manipulation of the animal. For this project, we tested the hypothesis that administration of the organism by a hematogenous route at gestational day (gd) 14 would result in increased tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 production by the placenta. STUDY DESIGN: Timed-pregnant, Sprague-Dawley rats were anesthetized on gd 14 and 10(7) CFU of M. pulmonis strain X1048 or an equivalent volume of sterile medium was injected into the heart. Rats were necropsied on gd 18 or 21, and ex vivo production of TNF-alpha and IL-6 was evaluated from six randomly selected placentas from each litter. The remaining placentas were harvested and either snap-frozen or placed in formalin. Frozen placentas were processed for real-time reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of TNF-alpha and IL-6 mRNA. Formalin-fixed placentas were sectioned and stained with hematoxylin and eosin for lesion analysis. RESULTS: Concentrations of TNF-alpha but not IL-6 were significantly higher in conditioned medium from placentas harvested from infected dams at gd 21. Levels of mRNA for IL-6 and TNF-alpha, however, were increased by M. pulmonis at gd 18 and 21. Analysis of gd 21 placentas by light microscopy revealed that significant histological chorioamnionitis was present in infected animals with accumulations of neutrophils in the capsular decidua. CONCLUSION: These data indicate that experimental infection with M. pulmonis causes histological chorioamnionitis, elevated mRNA levels of TNF-alpha and IL-6 in placental tissues, and the secretion of TNF-alpha by the placenta during late gestation.

Animals↗
PubMed2003

Store-operated Ca2+ entry in first trimester and term human placenta.

We have examined whether store-operated Ca2+ entry, a common pathway for Ca2+ entry in non-excitable tissue, is apparent in the syncytiotrophoblast of both first trimester and term human placenta. Expression of transient receptor potential (TRPC) homologues, a family of channels thought to be involved in store-operated Ca2+ entry, was also studied at the mRNA and protein levels. [Ca2+]i in syncytiotrophoblast of first trimester and term placental villous fragments was measured by microfluorimetry using the Ca2+-sensitive dye fura-2. Store-operated Ca2+ entry was stimulated using 1 microM thapsigargin in Ca(2+)-free Tyrode buffer (no added Ca2+ + 1 mM EGTA) followed by superfusion with control (Ca2+-containing) buffer. In term fragments, this protocol resulted in a rapid increase in [Ca2+]i, which was inhibited in the presence of 150 microM GdCl3, 200 microM NiCl2, 200 microM CoCl2 or 30 microM SKF96365 but was unaffected by addition of 10 microM nifedipine. It was not possible to stimulate such a rise in [Ca2+]i in first trimester fragments. Messenger RNA encoding TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 was identified in both first trimester and term placentas. From Western blotting, TRPC3 and TRPC6 proteins were detected in term, but not in first trimester, placentas, while TRPC1 protein was not detected. By immunocytochemistry, TRPC3 and TRPC4 were localised to cytotrophoblast cells in first trimester placentas and to the syncytiotrophoblast in term placentas. TRPC6 staining was present in the syncytiotrophoblast of both first trimester and term placenta, but the intensity was much greater in the latter. We propose that store-operated Ca2+ entry may be an important route for Ca2+ entry into the syncytiotrophoblast of term, but not first trimester placentas, and that in human placenta TRPC channels may underlie this entry mechanism.

Adult↗
PubMed1996

Increase in the relative level of type V collagen during development and ageing of the placenta.

AIM: To obtain some insight into the extracellular matrix in the placenta, changes in the composition of collagens during placental development were investigated. METHODS: Collagen was extracted from placentas (group 1, 25-30 weeks, n = 21; group 2, 31-36 weeks, n = 32; and group 3, 37-41 weeks of gestation, n = 40) and the relative concentrations of various collagens were evaluated by SDS-PAGE. RESULTS: The ratio of the intensity of the alpha 1 (III) band to that of alpha 1 (I) chain collagen in group 3 placentas were lower than those in group 1 placentas. In contrast, the ratio of the intensity of the alpha 1 (V) band to that of alpha 1 (I) chain collagen in group 3 placentas were higher than those in group 1 and group 2 placentas. CONCLUSIONS: These results suggest that type V collagen might play an important role in the function of the placenta and that an increased relative concentration of type V collagen might be closely associated with the development and ageing of the placenta.

Adult↗