Molecular Changes on Maternal-Fetal Interface in Placental Abruption-A Systematic Review.
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ABSTRACT:
SUBMITTER: Baczkowska M
PROVIDER: S-EPMC8235312 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ResultsAbruption cases were more likely to experience preeclampsia, have shorter gestational age, and deliver infants with lower birthweight compared with controls. Models with MFGI effects provided improved fit than models with only maternal and fetal genotype main effects for SNP rs12530904 (p-value = 1.2e-04) in calcium/calmodulin-dependent protein kinase [CaM kinase] II beta (CAMK2B), and, SNP rs73136795 (p-value = 1.9e-04) in peroxisome proliferator-activated receptor-gamma (PPARG), both MB genes. We identified 320 SNPs in 45 maternally-imprinted genes (including potassium voltage-gated channel subfamily Q member 1 [KCNQ1], neurotrimin [NTM], and, ATPase phospholipid transporting 10 A [ATP10A]) associated with abruption. Top hits included rs2012323 (p-value = 1.6E-16) and rs12221520 (p-value1.3e-13) in KCNQ1, rs8036892 (p-value = 9.3E-17) and rs188497582 in ATP10A, rs12589854 (p-value = 2.9E-11) and rs80203467 (p-value = 4.6e-11) in maternally expressed 8, small nucleolar RNA host (MEG8), and rs138281088 in solute carrier family 22 member 2 (SLC22A2) (p-value = 6.8e-9).ConclusionsWe identified novel PA-related maternal-fetal MB gene interactions and imprinting effects that highlight the role of the fetus in PA risk development. Findings can inform mechanistic investigations to understand the pathogenesis of PA.
| S-EPMC8601203 | biostudies-literature
Project description:Placental abruption and cardiovascular disease (CVD) have common etiological underpinnings, and there is accumulating evidence that abruption may be associated with future CVD. We estimated associations between abruption and coronary heart disease (CHD) and stroke. The meta-analysis was based on the random-effects risk ratio (RR) and 95% confidence interval (CI) as the effect measure. We conducted a bias analysis to account for abruption misclassification, selection bias, and unmeasured confounding. We included 11 cohort studies comprising 6,325,152 pregnancies, 69,759 abruptions, and 49,265 CHD and stroke cases (1967-2016). Risks of combined CVD morbidity-mortality among abruption and nonabruption groups were 16.7 and 9.3 per 1,000 births, respectively (RR = 1.76, 95% CI: 1.24, 2.50; I2 = 94%; τ2 = 0.22). Women who suffered abruption were at 2.65-fold (95% CI: 1.55, 4.54; I2 = 85%; τ2 = 0.36) higher risk of death related to CHD/stroke than nonfatal CHD/stroke complications (RR = 1.32, 95% CI: 0.91, 1.92; I2 = 93%; τ2 = 0.15). Abruption was associated with higher mortality from CHD (RR = 2.64, 95% CI: 1.57, 4.44; I2 = 76%; τ2 = 0.31) than stroke (RR = 1.70, 95% CI: 1.19, 2.42; I2 = 40%; τ2 = 0.05). Corrections for the aforementioned biases increased these estimates. Women with pregnancies complicated by placental abruption may benefit from postpartum screening or therapeutic interventions to help mitigate CVD risks.
| S-EPMC8796796 | biostudies-literature
Project description:Emerging data suggest that a trophoblast stem cell (TSC) population exists in the early human placenta. However, in vitro stem cell culture models are still in development and it remains under debate how well they reflect primary trophoblast (TB) cells. The absence of robust protocols to generate TSCs from humans has resulted in limited knowledge of the molecular mechanisms that regulate human placental development and TB lineage specification when compared to other human embryonic stem cells (hESCs). As placentation in mouse and human differ considerably, it is only with the development of human-based disease models using TSCs that we will be able to understand the various diseases caused by abnormal placentation in humans, such as preeclampsia. In this review, we summarize the knowledge on normal human placental development, the placental disease preeclampsia, and current stem cell model systems used to mimic TB differentiation. A special focus is given to the transforming growth factor-beta (TGF?) family as it has been shown that the TGF? family has an important role in human placental development and disease.
| S-EPMC7175362 | biostudies-literature
Project description:ObjectiveThe purpose of this study was to gain insight into the pathways that are associated with inflammation at the maternal-fetal interface. This study examined the molecular characteristics of monocytes that were derived from the maternal circulation and the placenta of obese women.Study designMononuclear cells were isolated from placenta, venous maternal, and umbilical cord blood at term delivery; activated monocytes were separated with CD14 immunoselection. The genotype and expression pattern of the monocytes were analyzed by microarray and real-time reverse transcriptase-polymerase chain reaction.ResultsThe transcriptome of the maternal blood and placental CD14 monocytes exhibited 73% homology, with 10% (1800 common genes) differentially expressed. Genes for immune sensing and regulation, matrix remodeling, and lipid metabolism were enhanced 2-2006 fold in placenta, compared with maternal monocytes. The CD14 placental monocytes exhibited a maternal genotype (9% DYS14 expression) as opposed to the fetal genotype (90% DYS14 expression) of the trophoblast cells.ConclusionCD14 monocytes from the maternal blood and the placenta share strong phenotypic and genotypic similarities with an enhanced inflammatory pattern in the placenta. The functional traits of the CD14 blood and placental monocytes suggest that they both contribute to propagation of inflammation at the maternal-fetal interface.
| S-EPMC3217185 | biostudies-literature
Project description:While available evidence supports the role of genetics in the pathogenesis of placental abruption (PA), PA-related placental genome variations and maternal-placental genetic interactions have not been investigated. Maternal blood and placental samples collected from participants in the Peruvian Abruptio Placentae Epidemiology study were genotyped using Illumina's Cardio-Metabochip platform. We examined 118,782 genome-wide SNPs and 333 SNPs in 32 candidate genes from mitochondrial biogenesis and oxidative phosphorylation pathways in placental DNA from 280 PA cases and 244 controls. We assessed maternal-placental interactions in the candidate gene SNPS and two imprinted regions (IGF2/H19 and C19MC). Univariate and penalized logistic regression models were fit to estimate odds ratios. We examined the combined effect of multiple SNPs on PA risk using weighted genetic risk scores (WGRS) with repeated ten-fold cross-validations. A multinomial model was used to investigate maternal-placental genetic interactions. In placental genome-wide and candidate gene analyses, no SNP was significant after false discovery rate correction. The top genome-wide association study (GWAS) hits were rs544201, rs1484464 (CTNNA2), rs4149570 (TNFRSF1A) and rs13055470 (ZNRF3) (p-values: 1.11e-05 to 3.54e-05). The top 200 SNPs of the GWAS overrepresented genes involved in cell cycle, growth and proliferation. The top candidate gene hits were rs16949118 (COX10) and rs7609948 (THRB) (p-values: 6.00e-03 and 8.19e-03). Participants in the highest quartile of WGRS based on cross-validations using SNPs selected from the GWAS and candidate gene analyses had a 8.40-fold (95% CI: 5.8-12.56) and a 4.46-fold (95% CI: 2.94-6.72) higher odds of PA compared to participants in the lowest quartile. We found maternal-placental genetic interactions on PA risk for two SNPs in PPARG (chr3:12313450 and chr3:12412978) and maternal imprinting effects for multiple SNPs in the C19MC and IGF2/H19 regions. Variations in the placental genome and interactions between maternal-placental genetic variations may contribute to PA risk. Larger studies may help advance our understanding of PA pathogenesis.
| S-EPMC4280220 | biostudies-literature
Project description:BackgroundIntra-uterine growth restriction (IUGR) and fetal overgrowth increase risks to postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying the effects of maternal nutrition on fetal development are not entirely clear. We developed a pig model, and using isobaric tags for relative and absolute quantification (iTRAQ), we investigated alterations in the placental proteome of gilts on a normal-energy-intake (Con) and high-energy-intake (HE) diet.ResultsIn the Con group, heavy and light fetuses were found at the tubal and cervical ends of the uterus respectively at 90 d of gestation. Moreover, the heavy fetuses had a higher glucose concentration than the light fetuses. However, a higher uniformity was noted in the HE group. Placental promoters between these two positions indicated that 78 and 50 differentially expressed proteins were detected in the Con and HE groups respectively. In the Con group, these proteins were involved in lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1), and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, in the HE group they mainly participated in transcriptional and translational regulation, and intracellular vesicular transport.ConclusionsOur findings revealed that maternal nutrition may alter birth weight mainly through the modulation of placental lipid and energy metabolism, which also provides a possible mechanism to explain the higher uniformity of fetal weight in gilts fed a HE diet.
| S-EPMC5331709 | biostudies-literature
Project description:ObjectiveWe hypothesized that the origins of abruption may extend to the stages of placental implantation; however, there are no reliable markers to predict its development. Based on this hypothesis, we sought to evaluate whether first-trimester and second-trimester serum analytes predict placental abruption.MethodsWe performed a secondary analysis of data of 35,307 women (250 abruption cases) enrolled in the First and Second Trimester Evaluation of Risk cohort (1999-2003), a multicenter, prospective cohort study. Percentiles (based on multiples of the median) of first-trimester (pregnancy-associated plasma protein A and total and free β-hCG) and second-trimester (maternal serum alpha-fetoprotein, unconjugated estriol, and inhibin-A) serum analytes were examined in relation to abruption. Associations are based on risk ratio (RR) and 95% confidence interval (CI).ResultsWomen with an abnormally low pregnancy-associated plasma protein A (fifth percentile or less) were at increased risk of abruption compared with those without abruption (9.6% compared with 5.3%; RR 1.9, 95% CI, 1.2-2.8). Maternal serum alpha-fetoprotein 95th percentile or greater was more common among abruption (9.6%) than nonabruption (5.1%) pregnancies (RR 1.9, 95% CI 1.3-3.0). Inhibin-A fifth percentile or less (8.0% compared with 5.1%; RR 1.8, 95% CI 1.1-2.9), and 95th percentile or greater (9.6% compared with 5.0%; RR 2.0, 95% CI 1.3-3.1) were associated with abruption. Women with all three abnormal pregnancy-associated plasma protein A, maternal serum alpha-fetoprotein, and inhibin-A analytes were at 8.8-fold (95% CI 2.3-34.3) risk of abruption. No associations were seen with other analytes.ConclusionThese data provide support for our hypothesis that the origins of placental abruption may extend to the early stages of pregnancy.
| S-EPMC5367463 | biostudies-literature
Project description:BackgroundPlacental abruption is an important cause of maternal and fetal mortality and morbidity.ObjectivesTo assess the effectiveness and safety of any intervention for the care of women and/or their babies following a diagnosis of placental abruption.Search strategyComprehensive electronic search of the Cochrane Pregnancy and Childbirth trials register. Date of last search: October 2002.Selection criteriaRandomised and 'quasi-randomised' trials that report clinically meaningful outcomes and present results on an intention to treat basis.Data collection and analysisIf eligible trials were to be identified, data will be extracted, unblinded, by the reviewer from all studies.Main resultsNo studies that met the inclusion criteria were identified.Reviewer's conclusionsThe clinical management of placental abruption has to rely on knowledge other than that obtained through randomised clinical trials.
| S-EPMC8711592 | biostudies-literature
Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.
2018-10-26 | PXD004951 | Pride
Project description:Placental abruption (early separation of the placenta) is associated with preterm birth and perinatal mortality, but associations with other neonatal morbidities remain understudied. We examined the association between abruption and newborn outcomes. We analyzed 223,341 singleton deliveries from the Consortium on Safe Labor study, a retrospective, multisite, observational study (2002-2008) of electronic medical records in the United States. Adjusted relative risks, incidence rate ratios, and 99% confidence intervals were estimated. Direct effects attributable to abruption were examined by conditioning on intermediates (preterm birth and small for gestational age) with sensitivity analyses. Incidence of abruption was 1.6% (n = 3,619). Abruption was associated with an elevated risk of newborn resuscitation (relative risk (RR) = 1.5, 99% confidence interval (CI): 1.5, 1.6), apnea (RR = 5.8, 99% CI: 5.1, 6.5), asphyxia (RR = 8.5, 99% CI: 5.7, 11.3), respiratory distress syndrome (RR = 6.5, 99% CI: 5.9, 7.1), neonatal intensive care unit admission (RR = 3.4, 99% CI: 3.2, 3.6), longer intensive care length of stay (incidence rate ratio = 2.0, 99% CI: 1.9, 2.2), stillbirth (RR = 6.3, 99% CI: 4.7, 7.9), and neonatal mortality (RR = 7.6, 99% CI: 5.2, 10.1). In sensitivity analyses, there was a direct effect of abruption associated with increased neonatal risks. These findings expand our knowledge of the association between abruption and perinatal and neonatal outcomes.
| S-EPMC5860509 | biostudies-literature