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.

SourceResearch connectionFrom yearThrough year

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

At least 343 records · Page 19Linked to original sources

PubMed1992

Diagnosis of placenta previa during the third trimester: role of transperineal sonography.

Placenta previa can be difficult to diagnose with transabdominal sonography during the third trimester of pregnancy, because of difficulties in imaging the cervix late in pregnancy. Although transperineal sonography offers an additional view of the cervix, its value in the diagnosis of placenta previa has not been studied. Accordingly, we performed transperineal sonography on 164 patients who had had transabdominal scans that had shown placenta previa or had been inconclusive during the third trimester of pregnancy. Transabdominal sonograms had been inconclusive for placenta previa in 157 of these patients because the cervix was not visualized. The remaining seven patients had transabdominal scans that showed placenta previa. Transperineal sonography successfully visualized the internal surface of the cervix in all 164 patients, allowing determination of the presence or absence of placenta previa in all cases. Transperineal sonograms showed absence of placenta previa in 154 patients. At delivery, none of these patients had evidence of placenta previa. Transperineal sonography showed placenta previa in 10 patients. In nine of these patients, placenta previa was confirmed at delivery. The 10th patient did not have clinically significant placenta previa at delivery. Our study shows that transperineal sonography is a valuable technique to complement transabdominal sonography for detection of placenta previa during the third trimester of pregnancy. Use of transperineal sonography should be strongly considered when a definitive diagnosis regarding placenta previa is not possible by transabdominal sonography because the cervix is not visualized. In such cases, transperineal sonography will usually show the internal surface of the cervix without overlying placental tissue, allowing confident exclusion of placenta previa. Occasionally, however, transperineal sonography will show a placenta previa that was not seen with transabdominal sonography.

Cervix Uteri↗

PubMed2006

[Involvement of matrix metalloproteinase-2, -9, and tissue inhibitors of metalloproteinase-1, 2 in occurrence of the accrete placenta].

OBJECTIVE: To investigate the roles of matrix metalloproteinase-9, -2 (MMP-9, 2), and tissue inhibitors of metalloproteinase-1, 2 (TIMP-1, 2) in pathogenesis of the accretio placenta. METHODS: The women with the placenta accrete were recruited and the placenta (23) and deciduas tissues (9) after labor were obtained, and the placenta (28) and deciduas (11) from women without the placenta accreta were obtained as control to get, too. The expressions of MMP-9, -2, TIMP-1, 2 in the placental and decidual tissues were analyzed by real-time PCR. RESULTS: mRNA expression of MMP-9 in the placenta accreta was (3.21 +/- 0.76) copies/microg total RNA, significantly higher (P < 0.05) than that of normal placenta [(3.84 +/- 0.24) copies/microg total RNA)]. MMP-9 transcription in the decidua accreta was (2.50 +/- 0.49) copies/microg total RNA, significantly higher (P < 0.05) than that of normal decidua [(3.81 +/- 0.66) copies/microg total RNA]. mRNA expression of TIMP-1 in normal placenta and placenta accreta was (5.91 +/- 0.56) and (5.92 +/- 0.46) copies/microg total RNA, respectively, with no significant difference between the two groups. mRNA expression of TIMP-1 in the accrete deciduas was (6.63 +/- 0.51) copies/microg total RNA, significantly lower (P < 0.05) than that of normal decidua (7.09 +/- 0.55) copies/microg. mRNA expression of MMP-2 in the accrete placenta was (4.55 +/- 1.13) copies/microg total RNA, significantly higher (P < 0.05) than that of normal placenta (5.53 +/- 0.59) copies/microg. mRNA expression of MMP-2 in the accrete decidua and normal decidua was (6.07 +/- 0.83) and (5.97 +/- 0.76) copies/microg total RNA, respectively, with no significant difference between the two groups. mRNA expression of TIMP-2 in the accrete placenta was (4.69 +/- 0.60) copies/microg total RNA, significantly higher (P < 0.05) than that of normal placenta (3.79 +/- 1.06) copies/microg. mRNA expression of TIMP-2 in the accrete decidua was (5.06 +/- 0.33) copies/microg total RNA, higher significantly (P < 0.05) than that of normal decidua (3.98 +/- 0.60) copies/microg. CONCLUSIONS: The upregulation of MMP-9, MMP-2 in placenta and downregulation of TIMP-1 in decidua were involved in occurrence of the placental accreta, and the roles of TIMP-2 in occurrence of the placental accreta need to elucidated.

Adult↗

PubMed2005

Expression of von Hippel Lindau (pVHL) protein in placentae from normal pregnant women and women with preeclampsia.

The hypoxia inducible transcription factors, HIF-1alpha and -2alpha proteins, are overexpressed in placentae from women with preeclampsia (Biol Reprod 2001;64:499-506; Biol Reprod 2001;64:1019-1020). Normally, these proteins are regulated in an oxygen-dependent manner being rapidly degraded by the ubiquitin-mediated proteasomal pathway. Recent studies have shown that the tumor suppressor protein, von Hippel Lindau (VHL), targets HIF for ubiquitinylation under nonhypoxic conditions. The objectives of the present work were: (1) to investigate VHL protein expression in normal pregnant (NP), preeclamptic (PE), and preterm (without PE) placentae, (2) to test whether VHL protein is hypoxia inducible in term and first trimester placental villous explants, and (3) to analyze the ontogeny of VHL protein expression in the human placenta. To begin evaluating the potential contribution of VHL to HIF overexpression in preeclamptic placentae, we analyzed the levels of the VHL protein in both normal and preeclamptic placentae (n=7 each). We hypothesized a deficiency of VHL protein in preeclamptic placentae. Eight biopsy sites were tested in each placenta and protein extracts were made. Western analysis was performed using VHL specific antibodies. Human renal adenocarcinoma (ACHN) cell extracts and extracts from COS-7 cells transfected with a VHL expression vector were used as positive controls. In a total of 112 biopsy sites that were analyzed (56 each for normal and preeclamptic placentae), the composite densitometry ratios (PE/NP) for the long (28 kDa) and short (19 kDa) forms of VHL were 1.09+/-0.2 and 1.16+/-0.11, respectively (both p=NS vs 1.0). A ratio of 1.0 indicates equal expression by preeclamptic and normal placentae. The same placentae exhibited composite densitometry (PE/NP) ratios of 1.97+/-0.23 and 1.68+/-0.20 for HIF-1alpha and -2alpha proteins, respectively (both p<0.05 vs 1.0). In a separate analysis, the protein expression of the short form of VHL was also comparable among NP, PE and preterm (n=6) placentae. VHL immunoreactivity was localized to cells within the basal plate and the syncytiotrophoblast. Despite induction of HIF proteins by hypoxia in first and term villous explants, there was no significant upregulation of VHL proteins. Finally, the expression of both the short and long forms of VHL protein decreased with gestational age (both p<0.05 by ANOVA), and in villous tissue from first trimester placentae VHL immunoreactivity was predominantly localized to the cytotrophoblast. These results suggest that (1) deficiency of VHL protein does not account for HIF-alpha overexpression in preeclamptic placentae, (2) VHL protein is not regulated by hypoxia in either first trimester or term placental villous explants, and (3) VHL protein expression in the placenta decreases as a function of gestational age.

Adult↗

PubMed2002

The calpain system in human placenta.

The calpain system is involved in a number of human pathologies ranging from the muscular dystrophies to Alzheimer's disease. It is important, therefore, to be able to obtain and to characterize both mu-calpain and m-calpain from human tissue. Although human mu-calpain can be conveniently obtained from either erythrocytes or platelets, no readily available source of human m-calpain has been described. Human placenta extracts contain both mu-calpain and m-calpain in nearly equal proportions and in significant quantities (3-4 mg mu-calpain and 4-5 mg m-calpain/1000 g placenta tissue). Placenta also contains calpastatin that elutes off ion-exchange columns over a wide range of KCl concentrations completely masking the mu-calpain activity eluting off these columns and even partly overlapping m-calpain elution. Placenta mu-calpain requires 50-70 microM Ca2+ and placenta m-calpain requires 450-460 microM Ca2+ for half-maximal proteolytic activity. Western analysis of washed placenta tissue shows that placenta contains both mu- and m-calpain, although some of the mu-calpain in whole placenta extracts likely originates from the erythrocytes that are abundant in the highly vascularized placenta. Placenta calpastatin could not be purified with conventional methods. The most prominent form of calpastatin in Western analyses of placenta obtained as soon as possible after birth was approximately 48-51 kDa; partly purified preparations of placenta calpastatin also contained 48-51 and 70 kDa polypeptides. Human placenta extracts likely contain two different calpastatin isoforms, a 48-51 kDa "placenta calpastatin" and a 70 kDa erythrocyte calpastatin.

Adult↗

PubMed2001

Third-trimester transvaginal ultrasonography in placenta previa: does the shape of the lower placental edge predict clinical outcome?

OBJECTIVE: To evaluate the clinical significance of the shape of the lower placental edge in women with transvaginal sonographic diagnosis of placenta previa. DESIGN: A prospective observational study at a tertiary teaching hospital. POPULATION: A total of 104 women with confirmed transvaginal sonographic diagnosis of placenta previa before 32 weeks' gestation. METHODS: Initial transvaginal sonography was performed at between 28 and 32 weeks' gestation in 138 patients with either strong clinical suspicion or previous abdominal sonographic diagnosis of placenta previa in the early third trimester. The lower placental edge was found to be positioned over the internal cervical os in 33 women (complete previa) and within 3 cm from it in 71 women (low-lying placenta). Patients with low-lying placenta were followed up by serial transvaginal sonographic examinations until delivery; detailed information including the placental location (anterior or posterior), the distance of its edge from the internal cervical os and its thickness were recorded. The clinical outcomes of the 17 who had a thick-edge low-lying placenta were compared with those who had a thin-edge one (54 women). In patients with complete placenta previa, demographic data, the shape of the lower placental edge whenever transvaginal sonography visualized it, and the clinical outcomes were documented. The incidence of major complications in thick-edge or central placenta was compared to that in the thin-edge group. RESULTS: Women having a low-lying placenta with a thick edge had a significantly higher rate of antepartum hemorrhage (P = 0.0002), abdominal delivery (P = 0.02), abnormally adherent placenta (P = 0.012) and low birth weight (P = 0.006) than those in whom the placental edge was thin. Cesarean hysterectomy was required in six patients with complete placenta previa because of severe peripartum hemorrhage; all of them had either central or thick-edge placenta accreta. CONCLUSION: Women with placenta previa are at a relatively higher risk of developing complications if the lower placental edge is thick. Integration of the shape of the lower placental edge into transvaginal sonographic assessment of placenta previa may improve the prediction of mode of delivery and clinical outcome.

Adult↗

PubMed2003

The effect of placenta previa on neonatal mortality: a population-based study in the United States, 1989 through 1997.

OBJECTIVE: The purpose of the study was to explore the associations of placenta previa with preterm delivery, growth restriction, and neonatal survival. STUDY DESIGN: A retrospective cohort study was performed of live births in the United States (1989-1991 and 1995-1997) that used the national linked birth/infant death records from 22,368,235 singleton pregnancies. The diagnosis of previa was restricted to those live births that were delivered (> or =24 weeks) by cesarean delivery. We evaluated gestational age and birth weight-specific risk of neonatal deaths (within the first 28 days) in relation to placenta previa. Fetal growth was assessed in centiles of birth weight (<3rd, 3rd-4th, 5th-9th, 10th-90th, and >90th centile), adjusted for gestational age. All analyses were adjusted for the confounding effects of the year of delivery, maternal age, gravidity, education, prenatal care, marital status, and race/ethnicity. RESULTS: Placenta previa was recorded in 2.8 per 1000 live births (n = 61,711). Neonatal mortality rate was 10.7 with previa, compared with 2.5 per 1,000 among other pregnancies (relative risk, 4.3; 95% confidence interval, 4.0,4.8). At 28 to 36 weeks, babies born to women with placenta previa weighed, on average, 210 g lower than babies born to women without placenta previa (P <.001). Compared with babies born to women without previa, the risk of death from placenta previa was lower among preterm babies (<37 weeks of gestation), with a crossover at 37 weeks where the mortality rate was higher for babies born to women with placenta previa than for babies born to women without placenta previa. This crossover also persisted in an analysis by birth weight and term births (delivered at > or =37 weeks of gestation). Mortality rates for term births were higher among babies born to women with placenta previa than among babies born women without placenta previa who were at the 10th to 90th centile (relative risk, 1.9; 95% confidence interval, 1.3, 2.8), and those at >90th centile (relative risk, 3.6; 95% confidence interval, 1.3, 9.6). Among preterm births, however, placenta previa was not associated with increased neonatal mortality by fetal growth centiles. CONCLUSION: The risk of neonatal mortality was higher for babies born to women with placenta previa than for babies born to women without placenta previa who were delivered at > or =37 weeks of gestation. Pregnancies that are diagnosed with placenta previa must be monitored carefully, especially as they approach term.

Adult↗

PubMed1985

Inner-ring deiodination of 3,5,3'-triiodothyronine in the in situ perfused guinea pig placenta.

Broken cell preparations of rat and human placentas contain an inner (tyrosyl)-ring iodothyronine deiodinase enzyme with greatest activity when the substrate is 3,5,3'-triiodothyronine (T3). This report describes the deiodination of T3 in the intact placenta and the effect of sodium iopanoate (IA) and propylthiouracil (PTU) on T3 deiodination. Under nembutal anesthesia, the placenta of 60-65-d-old pregnant guinea pigs was surgically exposed, a single umbilical artery and the umbilical vein were cannulated, and the fetus was removed. In a temperature-controlled chamber (37 degrees C), the fetal side of the placenta was perfused through the umbilical artery at a rate of 1 ml/min with 3% bovine serum albumin Krebs-Henseleit buffer containing 0.14 nM outer ring labeled [125I]T3. Placenta effluent fractions were collected at timed intervals from the umbilical vein cannula throughout a 120-min perfusion period. The contents of the perfusion buffer and the various effluent fractions were analyzed for their iodothyronine content by high pressure liquid chromatography. In five experiments, the percent composition of 125I-labeled iodothyronines in the perfusion buffer and placenta effluent was 95.3 +/- 1.0 (mean +/- SE) and 70.2 +/- 2.1 for T3 (P less than 0.01), 2.5 +/- 0.7 and 20.1 +/- 1.8 for 3,3'-T2 (P less than 0.01), and 0 and 8.2 +/- 0.9 for 3'-T1. There was no difference between the percent [125I]iodide in the perfusion buffer and in the placenta effluents. When placentas were perfused with IA and [125I]T3, after perfusion with [125I]T3 alone, there was a significant increase (P less than 0.01) in the percent [125I]T3 in the placenta effluents, and a significant decrease in [125I]3,3'-T2 (P less than 0.01) and [125I]3'-T1 (P less than 0.01). In contrast, PTU did not affect the composition of labeled iodothyronines in the placenta effluents, despite the fact that the addition of PTU significantly (P less than 0.001) inhibits the inner-ring deiodination of [125I]T3 in human or guinea pig placenta microsomes in the presence of low (0.25 mM) concentrations of dithiothreitol. The present studies demonstrate that T3 is actively deiodinated in the inner ring to 3,3'-T2 by the intact guinea pig placenta. A portion of 3,3'-T2 is further deiodinated in the inner ring to generate 3'-T1. No outer ring deiodination of T3 was seen under the conditions employed. IA, but not PTU, inhibits T3 deiodination in the placenta perfused in situ. We conclude that the placenta is probably a site for fetal T3 metabolism.

Animals↗

PubMed2003

Obstetric risk factors associated with placenta previa development: case-control study.

AIM: To evaluate potential risk factors and perinatal outcome of pregnancies complicated with placenta previa in Croatian population of pregnant women recruited from the largest tertiary care perinatal center in Croatia. METHODS: This retrospective case-control study included a total of 202 singleton pregnancies with placenta previa during a 10-year study period and 1,004 randomly selected simple singleton controls. Data on potential risk factors for placenta previa development were carefully extracted from medical records, reviewed, and compared with a control group of women. Data were statistically analyzed with chi-square test and Mann-Whitney U test, and crude odds ratio (OR) with 95% confidence interval (95% CI) were provided. RESULTS: The incidence of placenta previa was 0.4%. Factors significantly associated with a placenta previa development were advanced maternal age (especially >34 years, even after adjustment for high parity), gravidity of 3 and more (OR, 4; 95% CI, 2.5-6.6), more than one previous delivery (OR, 2.76; 95% CI, 1.7-4.3), history of previous cesarean sections (OR, 2.0; 95% CI, 1.17-3.44), abortions (OR, 2.8; 95% CI, 2.04-3.83), and presence of various uterine abnormalities (OR, 8.5; 95% CI, 1.75-44.5). The risk was significantly increased after two previous cesarean sections (OR, 7.32; 95% CI, 2.1-25) and after one previous abortion (OR, 4.8; 95% CI, 2.7-8.3). No difference between the groups was found regarding the history of previous placenta previa, drug abuse, and male sex at birth. Smoking history was significantly less frequent in women with placenta previa than controls (16.3% vs 25.6%, chi-square=7.9, p=0.007). The main perinatal complication was preterm birth, with 14-fold higher risk in women with placenta previa. Preterm infants of mothers with placenta previa were more likely to have lower first- (6 vs 10, p<0.001) and fifth-minute median Apgar scores (8 vs 10, p<0.045). Term infants of mothers with placenta previa had significantly lower birth weight then their controls (3,300 vs 3,500 g, p<0.001). CONCLUSION: The most important obstetric factors for placenta previa development were advanced maternal age especially >34 years, 3 or more previous pregnancies, parity of 2 and more, rising number of previous abortions, and history of previous cesarean section, but not child sex at birth, history of drug abuse and previous placenta previa. Smoking cigarettes was significantly less frequent in women with placenta previa. Preterm delivery still remains the greatest problem in pregnancies complicated with placenta previa.

Adult↗

PubMed2004

Risk factors predisposing to abruptio placentae. Maternal and fetal outcome.

OBJECTIVE: Abruptio placentae is one of the leading causes of perinatal deaths. Abruptio placentae increase the neonatal morbidity and mortality. It is one of the recognized causes of low birth weight. The purpose of this study was to examine the risk factors for abruptio placentae together with the maternal and fetal outcome in a large population based data set. METHODS: All cases of abruptio placentae presented to the Department of Obstetrics, Wad Medani Teaching Hospital, Sudan during the period January 1997 through to December 2002 were collected. All infants born to those cases were also collected and analyzed as live birth or stillbirth. The live born infants were followed for one month to detect the neonatal deaths. The study also aimed to determine the predisposing factors for abruptio placentae. The study was designed as a case control study from live, singleton births and singleton fetal death. RESULTS: The total number of abruptio placentae collected during this period was 1028, while the total number of births during the same period was 15620 giving and incidence of 1028/15620 (6.5%) for abruptio placentae. The combined stillbirths and first month deaths were 20.2%. Abruptio placentae was associated with pre-eclampsia, diabetes, polyhydramnios and hypertension. Parity and maternal age were not associated with an increased incidence of abruption placentae. CONCLUSION: This study had the advantage of complete ascertainment of all reported cases of abruptio placentae during a period of 6-years. We found an increased risk for abruptio placentae associated with maternal diabetes, hypertension, pre-eclampsia and polyhydramnios. We found that infants born after abruptio placentae were small for gestational age and had lower Apgar scores than the control infants. The possibility of abruptio placentae should be considered by the clinician when managing pregnant women with any of those characteristics. Abruptio placentae should be managed in centers were there is advanced maternal and neonatal facilities.

Abruptio Placentae↗

PubMed1997

[Histochemical localization of nitric oxide synthase in the human placenta].

OBJECTIVES: To study localization, distribution and activity of nitric oxide synthase (NOS) in the human placenta and to speculate the action of nitric oxide (NO) during pregnancy. METHODS: NADPH-diaphorasc histochemical method was used to indicate the distribution, localization and activity of NOS in the placentae of normal term pregnancy (n = 21). Severe pregnancy induced hypertension (PIH) (n = 15), intrauterine growth retardation (IUGR) (n = 2) and villi of early pregnancy (n = 16). RESULTS: The NOS reactive product called blue formazan was found in most of syncytiotrophoblast (STr) and located in top of cells in severe PIH and IUGR placentae. In normal term placentae the blue formazan was found in STr and located in base of cells. The number of blue formazan was more than that of PIH and IUGR placentae. Endothelial cells of most capillaries of the terminal villi in severe PIH and IUGR placentae were found to be deposited with blue formazan, but in normal term pregnancy, blue formazan was found only on rare occasion. CONCLUSION: Distribution and localization of NOS in placentae of normal term pregnancy, severe PIH and IUGR cases and early villi are specific. The NOS activity of STr in severe PIH placentae and IUGR placentae are lower than that of normal term placentae. The distribution and localization of NOS within the STr in severe PIH placentae and IUGR placentae are different from those in normal term placentae. The low activity of NOS secreted by placenta may be relative to the pathogenesis of PIH and IUGR.

Adult↗

PubMed1997

The association of placenta previa with history of cesarean delivery and abortion: a metaanalysis.

OBJECTIVE: Our purpose was to determine the incidence of placenta previa based on the available epidemiologic evidence and to quantify the risk of placenta previa based on the presence and number of cesarean deliveries and a history of spontaneous and induced abortion. STUDY DESIGN: We reviewed studies on placenta previa published between 1950 and 1996 on the basis of a comprehensive literature search with use of MEDLINE and by identifying studies cited in the references of published reports. Studies were chosen for inclusion in the metaanalysis if the incidence of placenta previa and its cross-classification with either prior cesarean delivery or abortions (both spontaneous and induced) or both were available. We also extracted details about the study design (case-control or cohort study) and place where they were conducted (United States or other countries). Published case reports dealing with placenta previa and studies relating to abruptio placentae were excluded from this review. We also restricted the search to studies published in English. No attempts were made to locate any unpublished studies. Data from studies identified during the literature search were reviewed and abstracted by a single author. In case of discrepancies or when the information presented in a study was unclear, abstraction by a (blinded) second reviewer was sought to resolve the discrepancy. RESULTS: Data on the incidence of placenta previa and its associations with previous cesarean delivery and abortions were abstracted. Subgroup analyses were performed to identify potential sources of heterogeneity by study design and place where they were conducted. Statistical methods used for the metaanalysis included the fixed-effects logistic regression model, whereas potential sources of heterogeneity among studies were evaluated by fitting random-effects models. The tabulation of 36 studies identified a total of 3.7 million pregnant women, of whom 13,992 patients were diagnosed with placenta previa. The reported incidence of placenta previa ranged between 0.28% and 2.0%, or approximately 1 in 200 deliveries. Women with at least one prior cesarean delivery were 2.6 (95% confidence interval 2.3 to 3.0) times at greater risk for development of placenta previa in a subsequent pregnancy. The results varied by study design, with case-control studies showing a stronger relative risk (relative risk 3.8, 95% confidence interval 2.3 to 6.4) than cohort studies did (relative risk 2.4, 95% confidence interval 2.1 to 2.8). Four studies, encompassing 170,640 pregnant women, provided data on the number of previous cesarean deliveries. These studies showed a dose-response pattern for the risk of previa on the basis of the number of prior cesarean deliveries. Relative risks were 4.5 (95% confidence interval 3.6 to 5.5) for one, 7.4 (95% confidence interval 7.1 to 7.7) for two, 6.5 (95% confidence interval 3.6 to 11.6) for three, and 44.9 (95% confidence interval 13.5 to 149.5) for four or more prior cesarean deliveries. Women with a history of spontaneous or induced abortion had a relative risk of placenta previa of 1.6 (95% confidence interval 1.0 to 2.6) and 1.7 (95% confidence interval 1.0 to 2.9), respectively. Substantial heterogeneity in the results of the metaanalysis was noted among studies. CONCLUSION: There is a strong association between having a previous cesarean delivery, spontaneous or induced abortion, and the subsequent development of placenta previa. The risk increases with number of prior cesarean deliveries. Pregnant women with a history of cesarean delivery or abortion must be regarded as high risk for placenta previa and must be monitored carefully. This study provides yet another reason for reducing the rate of primary cesarean delivery and for advocating vaginal birth for women with prior cesarean delivery.

Abortion, Induced↗

PubMed1996

Insulin-like growth factor II affects the appearance and glycogen content of glycogen cells in the murine placenta.

The phenotype of mice with a targeted disruption of the insulin-like growth factor II gene (IGF-II null mice) is growth retardation of both fetus and placenta during the last two thirds of gestation (1). We have compared the placenta of IGF-II null and wild-type mice from days 9-18 of gestation. No morphological differences were detected until after day 12 of gestation, when a new population of placental cells, the glycogen cells, normally first appears. Fewer glycogen cells were present in the null placenta compared to the wild-type placenta on days 13, 15, and 18 of gestation. By day 15, glycogen cells constituted approximately 50% of the basal zone cells in the wild-type placenta, but only 20% of the basal zone cells in the null placenta (P < 0.01). By contrast, spongiotrophoblasts constituted 40% of the basal zone cells in the wild-type placenta and 70% of the basal zone cells in the null placenta. There were no differences in cell size at any time. These results suggest that glycogen cells do not efficiently differentiate in the absence of IGF-II. The differentiation of glycogen cells did not appear to be simply delayed in the null placenta, as the number of glycogen cells in the null placenta did not increase between days 15-18, and there was no change in the ratio of glycogen to spongiotrophoblasts in the basal zone (P > 0.50). The glycogen content of both spongiotrophoblasts and glycogen cells was significantly reduced in the null placenta, suggesting that IGF-II may be an important regulator of glycogen synthesis in the placenta. These results indicate that IGF-II regulates cell number in the placenta and may play an important role in the differentiation of glycogen cells and the production of glycogen by placental cells.

Animals↗

PubMed2000

Expression patterns of placenta growth factor in human melanocytic cell lines.

Expression patterns of the angiogenic placenta growth factor and its receptor neuropilin-1 were assessed in normal human melanocytes, SV40T-transformed melanocytes, and melanoma cells derived from primary and metastatic lesions. As determined by reverse transcription-polymerase chain reaction all primary and metastatic melanoma cell lines tested and SV40T-transformed melanocytes coexpressed two placenta growth factor splice variants (placenta growth factor-1 and -2) as well as neuropilin-1 mRNA. Placenta growth factor protein was detected in conditioned media derived from five of eight melanomas and from SV40T-transformed melanocytes. In contrast to melanoma cells, normal melanocytes did not express placenta growth factor mRNA at detectable levels and did not secrete placenta growth factor protein. By contrast, neuropilin-1 transcripts were detected in some of the normal melanocytes. Secretion of placenta growth factor by melanoma cells appeared to be constitutive because it was not affected by the addition of exogenous growth factors including insulin, epidermal growth factor, or basic fibroblast growth factor to culture media. Although melanoma cells expressed both, neuropilin-1 and flt-1, exogenous homodimeric placenta growth factor had no effect on melanoma cell growth. Similarly, placenta growth factor did not induce urokinase-type plasminogen activator production in these cells. These findings demonstrate that melanoma progression is accompanied by deregulated, constitutive placenta growth factor expression. Placenta growth factor, however, serves no apparent autocrine role in melanoma proliferation. Further studies are needed to define the relative contribution of placenta growth factor to the angiogenic properties of human melanomas.

Angiogenesis Inducing Agents↗

PubMed2003

Expression and localization of estrogen receptor-alpha protein in normal and abnormal term placentae and stimulation of trophoblast differentiation by estradiol.

Estrogens play an important role in the regulation of placental function, and 17-beta-estradiol (E2) production rises eighty fold during human pregnancy. Although term placenta has been found to specifically bind estrogens, cellular localization of estrogen receptor alpha (ER-alpha) in trophoblast remains unclear. We used western blot analysis and immunohistochemistry with h-151 and ID5 monoclonal antibodies to determine the expression and cellular localization of ER-alpha protein in human placentae and cultured trophoblast cells. Western blot analysis revealed a ~65 kDa ER-alpha band in MCF-7 breast carcinoma cells (positive control). A similar band was detected in five normal term placentae exhibiting strong expression of Thy-1 differentiation protein in the villous core. However, five other term placentae, which exhibited low or no Thy-1 expression (abnormal placentae), exhibited virtually no ER-alpha expression. In normal placentae, nuclear ER-alpha expression was confined to villous cytotrophoblast cells (CT), but syncytiotrophoblast (ST) and extravillous trophoblast cells were unstained. In abnormal placentae no CT expressing ER-alpha were detected. Normal and abnormal placentae also showed ER-alpha expression in villous vascular pericytes and amniotic (but not villous) fibroblasts; no staining was detected in amniotic epithelial cells or decidual cells. All cultured trophoblast cells derived from the same normal and abnormal placentae showed distinct ER-alpha expression in western blots, and the ER-alpha expression was confined to the differentiating CT, but not to the mature ST. Trophoblast cells from six additional placentae were cultured in normal medium with phenol red (a weak estrogen) as above (PhR+), or plated in phenol red-free medium (PhR-) without or with mid-pregnancy levels of E2 (20 nM). Culture in PhR- medium without E2 caused retardation of syncytium formation and PhR-medium with E2 caused acceleration of syncytium formation compared to cultures in PhR+ medium. These data indicate that the considerable increase in estrogen production during pregnancy may play a role, via the ER-alpha, in the stimulation of CT differentiation and promote function in normal placentae. This mechanism, however, may not operate in abnormal placentae, which show a lack of ER-alpha expression.

Cell Differentiation↗

PubMed2006

Early embryonic death-associated changes in genome-wide gene expression profiles in the fetal placenta of the cow carrying somatic nuclear-derived cloned embryo.

Successful somatic nuclear transfer-derived cloning has been reported in cattle; however, the cloned embryo is highly susceptible to death around day 60 of gestation leading to early embryonic loss. The early embryonic death is postulated to possibly arise in part from an atypical placentation. We have performed cDNA macroarray analysis using 3,353 of the previously cataloged 4,165 genes, in order to characterize the early embryonic death-associated changes in genome-wide gene expression profiles in the fetal placenta of the cow carrying somatic nuclear transfer-derived cloned embryo. A more marked difference in the expression profiles was observed between the fetal placentas of the cows with the cloned immotile embryo (CD) and with the cloned motile embryo (CL) or artificial insemination-derived motile embryo (AI), as compared to between the CL and AI placentas, suggesting an aberration of the expression profile in the CD placenta among the three placentas. Further, 291 and 77 genes showed more than twofold elevation and less than 50% reduction, respectively, in either or both of two CD (CD1 and CD2) placentas in comparison with the CL placenta, but no differential expression between the CL and AI placentas. The expression patterns of six genes in the AI, CL, and CD placentas were confirmed in an experiment with an additional sample for each of the three placentas. Among the placental genes showing the early embryonic death-associated changes of expression in the cow with the cloned embryo, IGF2 (elevated gene), and HBA1, HBA2, SPTB, and SPTBN1 genes (reduced gene) are intriguing in that the changes of expression in these genes were observed in an additional sample of CD placenta as well as the CD1 and CD2 placentas, and in that overexpression (for IGF2) and dysfunction or deficiency (for HBA1, HBA2, SPTB, and SPTBN1) result in embryonic lethality.

Animals↗

PubMed1994

Second trimester sonographically diagnosed placenta previa: prediction of persistent previa at birth.

OBJECTIVES: We sought to determine the natural history of second trimester sonographically diagnosed placenta previa, and to ascertain whether the position of the placenta with respect to the cervical os at second trimester sonography can accurately predict persistence of the placenta previa at term. METHODS: The study population included all women consecutively diagnosed by ultrasound with placenta previa between 14 and 20 weeks' gestation. Medical records of the patients requiring cesarean section were reviewed to determine the presence of placenta previa. We reviewed the second trimester sonogram of patients who underwent abdominal delivery for placental and nonplacental indications to determine whether the central (symmetrical) versus the partial (asymmetrial) position of the placenta with respect to the internal os predicted the presence of placenta previa at delivery. RESULTS: A total of 925 second trimester- patients were sonographically identified as having placenta previa. Two hundred and sixty seven patients underwent cesarean delivery, 43 of which had placenta previa (43/925 or 4.6%). Twenty-two of the 43 were asymptomatic without antepartum bleeding. Analysis of the second trimester position of the placenta revealed that symmetry of the placenta with respect to the internal os at second trimester scan had a sensitivity of 49% for prediction of placenta previa at birth. CONCLUSIONS: The degree of placental symmetry with respect to the internal os during the second trimester successfully predicted the previas most likely to persist at delivery with a sensitivity of 49% (95% CI 34-64) and specificity of 93%.

Cesarean Section↗

PubMed1998

Equine retained placenta: technique for and tolerance to umbilical artery injections of collagenase.

Under laboratory conditions and in clinical experiments, bacterial collagenase has proven to be effective in hydrolyzing placenta and detaching cotyledon from caruncle in the bovine species. Laboratory studies in which placental samples were incubated with collagenase have also demonstrated that collagenase is 3.7 times more effective in hydrolyzing equine placenta than bovine placenta. This led to the hypothesis that collagenase may be a potential treatment for mares with retained placenta. However, that collagenase may hydrolyze the uterine wall and perforate the uterus was a concern. It was the purpose of this study thus to determine any adverse effects of collagenase on the equine uterus and to develop a method for intraplacental injection of collagenase. Three normally expelled intact placentas from Arabian mares, 10 cyclic mixed-breed mares, and 4 mares of various breeds with retained placenta were used. Fluoroscein dye and latex were used to study the placental vasculature and to determine a suitable dose of collagenase; placentas were hydrolyzed by collagenase solution in vitro. Bacterial collagenase solution (40,000 units, 200 ml) was infused into the uterine lumen of each cyclic mare. Uterine biopsies were obtained from the mares before collagenase infusion and again at 16 h and 26 d after infusion. In the mares with retained placenta, each placenta was infused via its umbilical cord vessels with 200,000 units of bacterial collagenase in 1 L of saline. Results showed that none of the uteri from cyclic mares were damaged by collagenase treatment. During a 4-wk period of monitoring (including endoscopy) mares with retained placenta did not show any abnormalities. Retained placentas were expelled in less than 6 h after collagenase treatment. It was concluded that intraplacental injections of collagenase are a safe and potentially effective treatment for retained placenta in mares.

Animals↗

PubMed1996

Production of granulocyte colony-stimulating factor by the human placenta at various stages of development.

The human placenta is capable of producing a variety of haematopoietic growth factors in vitro. It is not clear, however, whether the placenta produces such factors in vivo and if so, whether placental production of haematopoietic growth factors has a physiological role in fetal haematopoietic development. As a step toward making this determination, we assessed whether the onset of placental production of granulocyte colony-stimulating factor (G-CSF), in vivo, coincides with the onset of granulocytopoiesis in the developing fetus. To make this assessment, we obtained human placentae between 10 weeks of gestation and term and studied production of G-CSF in several ways. First, we sought to determine whether the onset of production of G-CSF mRNA in the placenta immediately precedes the appearance of neutrophil development in the fetus. Second, we assessed the effect of gestational age on the capacity of the placenta to generate G-CSF in vitro, by incubating cubes of placenta, with or without including interleukin-1 alpha (IL-1 alpha) in the culture media, and quantifying G-CSF in the cell culture supernatants 24 h later. Third, we assessed the rate of G-CSF production by the placenta, by perfusing two normal, term placentae using a membrane-oxygenator system, and quantifying G-CSF, at intervals, in the perfusates. We found: (1) no evidence that placental production of G-CSF is involved in regulating granulocytopoiesis in the fetus, (2) that the healthy placenta contains little or no G-CSF mRNA in vivo, (3) the placenta at term has a far greater capacity to produce G-CSF, when stimulated, than does the placenta before term, and (4) that although the placenta does not normally produce G-CSF in vivo, it has the capacity of generating very large quantities of G-CSF continuously over at least several days.

Blotting, Northern↗