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Placenta
Bailliere Tindall
Placenta

Bailliere Tindall

0143-4004

Placenta/Journal PlacentaSCIISTP
正式出版
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    Relationship between placental elastography, maternal pre-pregnancy body mass index and gestational weight gain

    Edwards C.Cavanagh E.Kumar S.Clifton V.L....
    6页
    查看更多>>摘要:? 2022Introduction: Maternal obesity is a significant risk factor for poor pregnancy outcomes. Obesity is linked to abnormalities in placental tissue at term. The purpose of this study was to correlate changes in placental stiffness, measured via ultrasound elastography, with maternal pre-pregnancy body mass index and gestational weight gain. Methods: Body Mass Index and gestation weight gain data was collected from 238 women. Elastography measurements were obtained via ultrasound at 24-, 28- and 36-weeks’ gestation. An analysis using a linear mixed regression model assessed for the statistical significance of pre-pregnancy BMI, pregnancy weight gain and placental SWV (Shear Wave Velocity). Results: Pre-pregnancy weight status has a significant impact on placental tissue stiffness detectable via ultrasound elastography. Placental tissue stiffness was highest in obese women, followed by overweight women. Obese women, on average, had a MeanSWV 0.11 m/s (95% CI (0.061–0.15) m/s, p < 0.001) above the healthy group throughout the 3rd trimester. Weight gain during pregnancy had a small impact on placental stiffness at the end of pregnancy. MeanSWV was 0.06 m/s (95% CI (0.03–0.10) m/s, p < 0.001) higher in the excessive weight gain group. Discussion: Structural changes of the placenta detected via ultrasound elastography techniques are not exclusive to placental dysfunction conditions (pre-eclampsia and growth restriction) but are also associated with maternal obesity.

    Second trimester uterine arteries pulsatility index is a function of placental pathology and provides insights on stillbirth aetiology: A multicenter matched case-control study

    Amodeo S.Cavoretto P.I.Seidenari A.Paci G....
    7页
    查看更多>>摘要:? 2022Introduction: The aim of this study was to investigate the relationships between maternal vascular malperfusions (MVM) and second trimester uterine arteries pulsatility index (UtA-PI) in cases of stillbirth (SB), compared to live-birth (LB) matched controls. Methods: This was a multicentre, observational, matched case-control study performed at five referral maternity centres over a 4-year period including SB and LB control pregnancies at high-risk for preeclampsia (PE) and/or fetal growth restriction (FGR), matched and stratified for UtA-PI MoM quartiles values of the SB cases. Logistic regression was used to assess the rates of each MVM finding, within each increasing MoM quartile subcategory in SB and matched LB controls. Results: 82 SB and 82 LB matched high-risk pregnancies were included. Placental hypoplasia, placental infarction, retroplacental hematoma, distal villous hypoplasia and accelerated villous maturation showed a significant correlation with UtA-PI. At univariable analysis, placental infarction and distal villous hypoplasia were more highly associated with the increasing quartile uterine Doppler measurements (odds ratio 2.24 and 2.23, respectively). Logistic regressions showed a significant positive and independent association between rates of retroplacental hematoma or distal villous hypoplasia and stillbirth within corresponding UtA-PI MoM quartiles (odds ratio 5.21 and 2.28, respectively). Discussion: We are providing evidence for characterization of two major etiological stillbirth categories, characterized by a positive or absent association with UtA-PI impairment and specific histopathological placental MVM lesions. Our results support a strict third trimester follow-up of cases with increased second trimester UtA-PI, in order to improve the reproductive chances of these pregnant patients.

    Assessing hypoxic damage to placental trophoblasts by measuring membrane viscosity of extracellular vesicles

    Huang C.Li H.Powell J.S.Ouyang Y....
    9页
    查看更多>>摘要:? 2022 Elsevier LtdIntroduction: As highly sophisticated intercellular communication vehicles in biological systems, extracellular vesicles (EVs) have been investigated as both promising liquid biopsy-based disease biomarkers and drug delivery carriers. Despite tremendous progress in understanding their biological and physiological functions, mechanical characterization of these nanoscale entities remains challenging due to the limited availability of proper techniques. Especially, whether damage to parental cells can be reflected by the mechanical properties of their EVs remains unknown. Methods: In this study, we characterized membrane viscosities of different types of EVs collected from primary human trophoblasts (PHTs), including apoptotic bodies, microvesicles and small extracellular vesicles, using fluorescence lifetime imaging microscopy (FLIM). The biochemical origin of EV membrane viscosity was examined by analyzing their phospholipid composition, using mass spectrometry. Results: We found that different EV types derived from the same cell type exhibit different membrane viscosities. The measured membrane viscosity values are well supported by the lipidomic analysis of the phospholipid compositions. We further demonstrate that the membrane viscosity of microvesicles can faithfully reveal hypoxic injury of the human trophoblasts. More specifically, the membrane of PHT microvesicles released under hypoxic condition is less viscous than its counterpart under standard culture condition, which is supported by the reduction in the phosphatidylethanolamine-to-phosphatidylcholine ratio in PHT microvesicles. Discussion: Our study suggests that biophysical properties of released trophoblastic microvesicles can reflect cell health. Characterizing EV's membrane viscosity may pave the way for the development of new EV-based clinical applications.

    Late selective termination and the occurrence of placental-related pregnancy complications: A case control study

    Weissbach T.Tal I.Regev N.Shust-Barequet S....
    9页
    查看更多>>摘要:? 2022 Elsevier LtdIntroduction: Multiple pregnancies are at increased risk of placental-related complications. The aim of the study was to investigate the prevalence and cumulative incidence of placental-related complications in twin pregnancies undergoing a late selective termination, compared to matched singleton and twin controls. Methods: A retrospective case-control study of post-selective late termination (≥20 weeks of gestation) singletons performed between 2009 and 2020 at a single tertiary center. Each post-termination pregnancy was matched to 2 singleton and 2 dichorionic twin pregnancies for: mode of conception, maternal age group and parity. The prevalence of composite placental related outcome was determined and compared. Kaplan-Meier curves were constructed, and log rank test was performed to compare the cumulative incidence of placental complications among groups. Results: Included were 90 post-selective termination pregnancies and 360 matched singletons and twins. These were subdivided according to trimester at procedure: 1) late 2nd trimester (N = 43, 20–27.6 weeks); 2) 3rd trimester (N = 47, ≥28 weeks). Placental-related complications presented earlier in the 3rd trimester selective termination group compared to singletons (median 35.5 vs median 37.4 weeks of gestation, P = 0.01). The cumulative incidence of placental-related complications in twins and post-selective termination singletons rose significantly earlier compared to singletons (P < 0.0001). A late 2nd trimester selective termination resulted in a comparable gestational age and cumulative incidence of placental-related complications as singletons. Discussion: Compared to singletons, the cumulative incidence of placental complications rises significantly earlier in post-third trimester selective termination singleton pregnancies. While a late 2nd trimester selective termination results in a cumulative incidence comparable to singletons.

    Crosstalk between foetal vasoactive peptide hormones and placental aminopeptidases regulates placental blood flow: Its significance in preeclampsia

    Yoshihara M.Mizutani S.Matsumoto K.Kato Y....
    8页
    查看更多>>摘要:? 2022In pregnancy, placental circulation occurs through two independent circulation systems: foetoplacental and uterine (spiral artery)-placental lake. Crosstalk between the foetal peptide hormones, angiotensin II (A-II) and vasopressin (AVP), and their degrading placental aminopeptidases (APs), aminopeptidase A for A-II and placental leucine aminopeptidase for both AVP and oxytocin, primarily regulate placental circulation. On the other hand, placental circulation represents an arteriovenous shunt. In normal pregnancy, the blood pressure decreases, despite increased cardiac output and plasma volume, probably due to the arteriovenous shunt in the growing placenta. Actually, the foetal vasoactive hormones in the foetoplacental circulation are much higher than those in the maternal circulation throughout pregnancy. In normal pregnancy, AP activity derived from the placenta in maternal blood increases with gestation and placental growth. Foetal hypoxia increases the secretion of foetal both AVP and A-II. Although there is an increase in both AP activities in the maternal blood in normal pregnancy, their activities increase more than those in normal pregnancy during mild preeclampsia. However, both AP activities decline significantly compared than those in severe preeclampsia. This suggests that AP prevents leakage of increased foetal vasoactive hormones into the maternal blood in mild preeclampsia, and its protective role breaks down in severe preeclampsia, leading to a massive leak of the hormones into maternal circulation and consequent marked contraction of both the maternal vessels and the uterus. Consequently, AP activity in both placenta and maternal blood acts as the foeto-maternal barrier for foetal vasoactive hormones and thus contributes to the onset of preeclampsia.

    Percentiles of intrauterine placental volume and placental volume relative to fetal volume: A prospective magnetic resonance imaging study

    Peterson H.F.Eskild A.Sommerfelt S.Gjesdal K....
    6页
    查看更多>>摘要:? 2022 The AuthorsIntroduction: We aimed to provide percentiles of intrauterine placental growth and placental growth relative to fetal growth (placental to fetal ratio) by measuring placental and fetal volumes by magnetic resonance imaging (MRI). Methods: In this prospective study, 107 unselected singleton pregnancies were examined by MRI at gestational week 27 and 37. Based on the estimated volumes of the placenta and the fetus, we calculated median and percentiles at gestational weeks 27 and 37. Results: Median placental volume at gestational week 27 was 513 cm3 (Inter Quartile Range (IQR) 182 cm3), and 831 cm3 (IQR 252 cm3) at week 37. The 10th – 90th percentiles included placental volumes between 392 and 717 cm3 at gestational week 27, and 631–1087 cm3 at week 37. The placental to fetal ratio was significantly higher at gestational week 27 than at week 37, with a median ratio of 0.54 (IQR 0.18) and 0.31 (IQR 0.08), respectively (p < 0.001). The 10th-90th percentiles included placental to fetal ratios between 0.43 and 0.73 at gestational week 27 and 0.25–0.39 at week 37. Discussion: At gestational week 27, the placental volume was about half the size of the fetal volume, whereas at week 37, the placental volume was about one third of the fetal volume. This finding suggests that placental growth was less prominent than fetal growth after gestational week 27. Knowledge about the distribution of intrauterine placental size in the general population of pregnancies are prerequisites for diagnosing abnormal placental size.

    Placental concentrations of alkali metals and their associations with neural tube defects in offspring

    Pi X.Wang D.Wang C.Li Z....
    7页
    查看更多>>摘要:? 2022 Elsevier LtdIntroduction: The role of alkali metals in the development of neural tube defects (NTDs) is little known. We examined the associations between placental concentrations of lithium (Li), sodium (Na), potassium (K), rubidium (Rb), and cesium (Cs), and the occurrence of NTDs in fetuses. Methods: 408 women who had NTD-affected pregnancies and 593 women who delivered healthy infants were included. Logistic regression, weight quantile sum regression (WQSR), and Bayesian kernel machine regression (BKMR) were applied to assess whether these metals are associated with the occurrence of NTDs. Results: Cs showed an inverse association with the odds of NTDs [adjusted odds ratio (aOR): 0.58, 95% confidence interval (CI): 0.36–0.91] in single-metal logistic model. Estimates did not change much in the multiple-metal logistic model. In WQSR, the WQS index was inversely associated with the odds of NTDs (aOR: 0.62, 95%CI: 0.51–0.75), in which Cs (weighted 0.45) had the highest weight. In BKMR, the odds of NTDs decreased with the levels of the five-metal mixtures. Cs was associated with decreased odds of NTDs when the remaining four metals were fixed at their 25th and 50th percentiles, while Na was associated with increased odds of NTDs when setting other metals at the 25th, 50th, or 75th percentile. Discussion: A high concentration of Cs and Na in placental tissue was respectively associated with decreased and increased odds of NTDs. In addition, the occurrence of NTDs decreased with the levels of the five-metal mixtures.

    Gene expression profiling of placentae from women with obesity and obstructive sleep apnoea

    Johns E.C.Halligan D.L.Tammsalu T.Hill E.A....
    8页
    查看更多>>摘要:? 2022Introduction: Obstructive sleep apnoea (OSA), a condition characterised by intermittent hypoxia and reoxygenation during sleep, is associated with an increased risk of adverse pregnancy outcomes including gestational diabetes and hypertensive disorders of pregnancy. The biological mechanisms of these associations are poorly understood. The impact of OSA on placental function has not been well characterised. Methods: We performed 3’ mRNA sequencing on placenta from women with obesity and OSA (n = 11) and women with obesity and no OSA (n = 9). Results: After correcting for multiple testing, there were no statistically significant differences in gene expression between OSA and no OSA groups (adjusted p < 0.05). In unadjusted analyses, 101 genes were differentially expressed in OSA compared to no OSA placentae (p < 0.01). In Reactome pathway and GO term analysis, this included downregulation of genes involved in O-linked glycosylation (B3GNT5 and B3GNT8) and Wnt signalling (TRABD2B and FRZB) pathways. In gene set enrichment analysis, genes within 24 pathways had a non-random distribution in OSA compared to no OSA placentae (adjusted p < 0.05). This included an increase in genes relating to the reversible hydration of carbon dioxide in OSA placentae, a potential novel mechanism contributing to the development of adverse pregnancy outcomes in women with OSA. Discussion: There is overall similarity in the placental transcriptome of women with obesity who do and do not have OSA during pregnancy. Alterations in the reversible hydration of carbon dioxide are a potential mechanism contributing to the development of adverse pregnancy outcomes in maternal OSA, however this finding requires validation in larger cohorts.

    Low-dose aspirin prevents LPS-induced preeclampsia-like phenotype via AQP-1 and the MAPK/ERK 1/2 pathway

    Xie H.Feng L.Zhang J.Jing S....
    9页
    查看更多>>摘要:? 2022Introduction: Clinical studies suggest that early pregnancy is the critical window for the prevention of preeclampsia by low-dose aspirin (LDA). Abnormal extravillous trophoblast (EVT) cell invasion and spiral artery remodeling during early placentation have been observed in preeclampsia cases. Thus, we hypothesized LDA prevents preeclampsia by mitigating EVT migration/invasion and spiral artery remodeling dysfunction. Methods: A single systemic lipopolysaccharide (LPS) (1 μg/kg) injection was administrated in pregnant mice at e14.5 to induce a preeclampsia-like pregnant mouse model. We administered LDA (2.5 μg/g body weight/day) and observed the effects on LPS-induced preeclampsia-like symptoms by examining the placental histology, protein expression, EVT invasion, and spiral artery remodeling. In human EVT cell line, HTR-8/SVneo, we investigated cell invasion and migration by matrigel and wound healing assays, respectively. Signaling pathways were surveyed using inhibitors, siRNA transfections, and Western blot. Results: LDA treatment significantly reversed the preeclampsia-like phenotype induced by LPS, as observed by decreases in hypertension, proteinuria, and fetal growth retardation. The numbers of pathological lesions, including excessive extracellular matrix deposition, endotheliosis, and collapsed glomerular capillaries in kidneys, were significantly lower in the LDA+LPS vs. the LPS group. LDA pretreatment eliminated placental lesions, including calcification, edema, and narrowed uterine spiral arteries and reduced aquaporin-1 (AQP-1) protein expression. In HTR-8/SVneo cells, LDA rescued the decreased cell migration and invasion induced by LPS. The phosphorylation of ERK1/2 was up-regulated and AQP-1 expression was decreased by LPS, which were reversed by LDA treatments. The effects of LDA were inhibited when AQP-1 expression was downregulated by siRNA transfection. Discussion: This study provides new evidence that supports the use of LDA for the prevention of preeclampsia and suggests that the effects of LDA are mediated through a novel mechanism of a water channel, AQP-1, and MAPK/ERK 1/2 signaling.

    Computational analysis identified accelerated senescence as a significant contribution to preeclampsia pathophysiology

    Siddique N.Cox B.
    9页
    查看更多>>摘要:? 2022 Elsevier LtdIntroduction: Preeclampsia is a heterogenous disorder of pregnancy that has distinct subtypes based on the phenotype of the placenta. In all pregnancies, there is a progressive loss of placental function throughout gestation due to increasing placental senescence. The aim of our study was to determine, through bioinformatic analyses, if accelerated or abnormal placental senescence underlies the development of the different subtypes of preeclampsia. Methods: Gene expression datasets were processed in R using the limma package for quantification and differential expression and the camera function for gene set enrichment. The pro- and anti-senescence gene sets were obtained from CellAge (https://genomics.senescence.info/cells/). Results: We demonstrate an overall downregulation of anti-senescence genes across healthy and preeclamptic placentas as a function of gestation that is accelerated in certain subtypes of preeclampsia. We also discovered that while senescence-related signatures are common to preeclampsia, they represented unique biological pathways to different subtypes of the disease. Discussion: Overall, our results support the role of senescence as a mediator in the pathophysiology of preeclampsia. We describe possible mechanistic differences between the role of senescence in different subtypes of preeclampsia that could provide a basis for identifying drug targets.