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Placenta Sep 2020We aim to examine the location of the vascular equator according to the umbilical cord insertions in monochorionic twin placentas.
INTRODUCTION
We aim to examine the location of the vascular equator according to the umbilical cord insertions in monochorionic twin placentas.
METHODS
We combined two prospective series of monochorionic diamniotic twin placentas of patients included in the first trimester between 2004 and 2008, and between 2016 and 2019. We injected the placentas after birth and divided them into three groups, with respectively concordant (eccentric-eccentric, marginal-marginal, and velamentous-velamentous), intermediate (eccentric-marginal and marginal-velamentous) and discordant (eccentric-velamentous) cord insertions. For each unidirectional anastomosis, we determined the cord-anastomosis ratio and then calculated the mean ratio per placenta in each group. We also calculated the deviation from the midline in all groups.
RESULTS
195 placentas were included. In concordant placentas, the mean cord-anastomosis ratio was 0.957 (95% CI [0.908-1.009]). In placentas with intermediate discordance, the mean ratio was 0.886 (95% CI [0.828-0.948]) and in discordant placentas it was 0.797 (95% CI [0,708-0.897]) (p < 0.001). In concordant placentas, the equator was in the middle of the cord insertions with an average deviation of 0.2 cm (95% CI [-0.1 - 0.3]). In the intermediate placentas, the equator deviated on average 0.5 cm (95% CI [0.2-0.8]) and was displaced from the middle towards the most central cord insertion. In discordant placentas, there was an average displacement of 1.0 cm (95% CI [0.50-1.6]).
DISCUSSION
In concordant placentas, the vascular equator lies in the middle between both cord insertions. In intermediate and discordant placentas, the equator is closer to the more central cord insertion.
Topics: Adult; Female; Fetofetal Transfusion; Humans; Laser Therapy; Placenta; Pregnancy; Twins, Monozygotic; Ultrasonography, Prenatal; Umbilical Cord
PubMed: 32988575
DOI: 10.1016/j.placenta.2020.05.008 -
Journal of Perinatology : Official... Apr 2019To determine if pre-specified placental abnormalities among newborns with hypoxic-ischemic encephalopathy (HIE) differ compared to newborns admitted to a NICU without...
OBJECTIVE
To determine if pre-specified placental abnormalities among newborns with hypoxic-ischemic encephalopathy (HIE) differ compared to newborns admitted to a NICU without encephalopathy.
STUDY DESIGN
Retrospective case-control study of newborns with HIE (2006-2014) and controls matched for birth year, gestational age, weight, and gender. One pathologist reviewed archived placental sections using pre-specified criteria.
RESULTS
Sixty-seven newborns had HIE, 46 had available placentas and were matched with 92 controls. HIE had more maternal vascular malperfusion (46% vs 25%, p = 0.02), fetal vascular malperfusion (13% vs 0%, p < 0.001), and clinical abruption (22% vs 4%, p = 0.001). Controls had more normal placentas (29% vs 7%, p = 0.002), and chorioamnionitis (30% vs 9%, p = 0.005). Pre-specified placental lesions occurred in 87% of HIE and 65% of controls (p = 0.008) and identified >90% of primary diagnoses.
CONCLUSIONS
Pre-specified placental lesions identified nearly all abnormalities in HIE and represented both acute and chronic processes.
Topics: Abruptio Placentae; Case-Control Studies; Female; Humans; Hypoxia-Ischemia, Brain; Infant, Newborn; Male; Placenta; Placental Circulation; Pregnancy; Retrospective Studies; Statistics, Nonparametric; Umbilical Cord
PubMed: 30770878
DOI: 10.1038/s41372-019-0334-9 -
Annals of Clinical and Laboratory... Mar 2021Fetal growth restriction (FGR) refers to impaired and insufficient intrauterine growth potential caused by a variety of adverse factors and is a serious perinatal...
OBJECTIVE
Fetal growth restriction (FGR) refers to impaired and insufficient intrauterine growth potential caused by a variety of adverse factors and is a serious perinatal complication that leads to fetal or neonatal mortality and morbidity. FGR has numerous causes, and its pathogenesis has not been fully understood. Recently, increasing numbers of researchers have begun to focus on the placenta, the only link between the fetus and the mother. The placenta is a vital organ that plays key roles in fetal development. PLAC1 is a trophoblast-specific gene located on the X chromosome and is important for placental development. However, the biological role of PLAC1 in fetal growth restriction is not well understood. In this study, we investigated the changes in the expression of placental-specific protein 1(PLAC1) in the placentas of pregnant women with FGR and in the placentas of normal pregnancies. We also explored the regulation of PLAC1 in the growth of trophoblast cells.
METHODS
Western blotting was used to detect the expression of PLAC1 in FGR and in normal placenta tissues. Cell counting kit 8 (CCK-8), wound healing, and transwell assays were used to detect the effects of PLAC1 knockdown on trophoblast cell proliferation, migration, and invasion. Western blotting was used to detect the expression of PLAC1 under hypoxic conditions, and the cell viability and apoptosis of trophoblast cells in a low oxygen concentration after overexpression of PLAC1 were detected by CCK-8 and flow cytometry assay.
RESULTS
Compared with the placentas in the control group of normal pregnancies, the expression of PLAC1 in the placentas of the FGR group was significantly down-regulated (<0.05). Knocking down PLAC1 by siRNA significantly inhibited the proliferation, migration, and invasion of trophoblast cells. After treatment with alow oxygen concentration, the expression of PLAC1 protein was significantly reduced (<0.05). The overexpression of PLAC1 can reverse the cell viability of trophoblast cells (<0.05) and inhibit apoptosis of trophoblast cells (<0.05) in low oxygen concentration.
CONCLUSION
The expression of PLAC1 was reduced in fetal growth restriction and did not protect trophoblast cells from hypoxic damage, suggesting that PLAC1 may be an important regulator in the occurrence of fetal growth restriction.
Topics: Adult; Apoptosis; Cell Line; Cell Movement; Cell Proliferation; China; Female; Fetal Growth Retardation; Humans; Placenta; Pregnancy; Pregnancy Proteins; Signal Transduction; Trophoblasts
PubMed: 33941557
DOI: No ID Found -
Magnetic Resonance in Medicine Aug 2018To assess which microstructural models best explain the diffusion-weighted MRI signal in the human placenta.
PURPOSE
To assess which microstructural models best explain the diffusion-weighted MRI signal in the human placenta.
METHODS
The placentas of nine healthy pregnant subjects were scanned with a multishell, multidirectional diffusion protocol at 3T. A range of multicompartment biophysical models were fit to the data, and ranked using the Bayesian information criterion.
RESULTS
Anisotropic extensions to the intravoxel incoherent motion model, which consider the effect of coherent orientation in both microvascular structure and tissue microstructure, consistently had the lowest Bayesian information criterion values. Model parameter maps and model selection results were consistent with the physiology of the placenta and surrounding tissue.
CONCLUSION
Anisotropic intravoxel incoherent motion models explain the placental diffusion signal better than apparent diffusion coefficient, intravoxel incoherent motion, and diffusion tensor models, in information theoretic terms, when using this protocol. Future work will aim to determine if model-derived parameters are sensitive to placental pathologies associated with disorders, such as fetal growth restriction and early-onset pre-eclampsia. Magn Reson Med 80:756-766, 2018. © 2017 The Authors Magnetic Resonance in Medicine published by Wiley Periodicals, Inc. on behalf of International Society for Magnetic Resonance in Medicine. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Topics: Anisotropy; Bayes Theorem; Diffusion Magnetic Resonance Imaging; Female; Humans; Image Processing, Computer-Assisted; Microcirculation; Placenta; Pregnancy
PubMed: 29230859
DOI: 10.1002/mrm.27036 -
Wiadomosci Lekarskie (Warsaw, Poland :... 2022The aim: The impact of undifferentiated connective tissue dysplasia on the formation of the placenta.
OBJECTIVE
The aim: The impact of undifferentiated connective tissue dysplasia on the formation of the placenta.
PATIENTS AND METHODS
Materials and methods: The morphostructure of 50 placentas with the undifferentiated connective tissue syndrome and 50 placentas of women with physiological pregnancy and absence of connective tissue pathology was studied.
RESULTS
Results: The results of morphological studies have shown that the main pathogenetic link of placental dysfunction with highly resistant blood flow in the umbilical arteries in pregnant women with undifferentiated connective tissue dysplasia syndrome is a disorder of functional differentiation of the villous tree.In these cases the dominats were large and medium-sized villi with narrowed lumen in arterial, venular and capillary vessels and arterial spasm and venous plethora, as well as with numerous chaotically sclerosed villi, indicating stage I and II of placental. There is a large amount of fibrins in intervillous space which narrows it and leads to violation of microcirculation and placenta tissue hypoxia.
CONCLUSION
Conclusions: The morphological basis of high flow resistance in the umbilical artery with the undifferentiated connective tissue dysplasia syndrome in pregnant women is a pathological immaturity of the placental villous tree. Morphological study of the architecture of the stem and intermediate placental villi revealed a violation of the structure of collagen fibers in the form of lack of crosslinks of bundles of collagen fibers.
Topics: Female; Pregnancy; Humans; Placenta; Chorionic Villi; Arteries; Collagen; Connective Tissue
PubMed: 36472281
DOI: 10.36740/WLek202210128 -
Placenta Feb 2021To explore the involvement of signal transducers and activators of transcription (STATs) in trophoblast differentiation.
INTRODUCTION
To explore the involvement of signal transducers and activators of transcription (STATs) in trophoblast differentiation.
METHODS AND RESULTS
First, the localization of STATs in human placentas was detected via immunohistochemistry (IHC) and immunofluorescence (IF). Cytotrophoblasts (CTBs) expressed both STAT1 and 3, but syncytiotrophoblasts (STBs) did not. Staining for these two proteins showed a distinct upregulation from the proximal part to the distal end of cell columns. STAT5B was mainly expressed in the STBs, low in the CTBs, and absent in the extravillous trophoblasts (EVTs). Next, the 44 placenta samples were tested via western blot (WB) and quantitative real time polymerase chain reaction (qRT-PCR). We found a decrease in STAT1 and 3 and an increase in STAT5B as gestation increased from five to 10 weeks. Then, an in vitro co-culture model of placenta with or without decidua stromal cells (DSCs), as detected via flow cytometry, revealed an increase in the human leukocyte antigen (HLA)-G positive rate in trophoblasts from placentas co-cultured with DSCs, accompanied by an increase in p-STAT1 and 3 and a decrease in p-STAT5 and STAT5B. Finally, mRNA of matrix metalloproteinases (MMPs) and integrins after STAT silencing in HTR-8/SVneo was detected via qRT-PCR. STAT1 silencing decreased MMP9 expression, STAT3 silencing decreased MMP9, integrin α6, and β4 expression, and STAT5B silencing increased MMP2 and integrin β1 expression.
DISCUSSION
Different trophoblasts showed distinct STAT expression profiles which were related to their MMP and integrin expression. DSCs promoted trophoblast differentiation into EVTs, possibly by regulating the STAT expression of the trophoblasts.
Topics: Adult; Cell Differentiation; Cell Line; Female; Humans; Matrix Metalloproteinases; Placenta; Pregnancy; STAT Transcription Factors; Stromal Cells; Trophoblasts; Young Adult
PubMed: 33556719
DOI: 10.1016/j.placenta.2021.01.021 -
Molecular and Cellular Biochemistry Jan 2018Altered placental angiogenesis is implicated in the pathophysiology of preeclampsia. We have earlier reported placental regional differences in oxidative stress markers... (Clinical Trial)
Clinical Trial
Altered placental angiogenesis is implicated in the pathophysiology of preeclampsia. We have earlier reported placental regional differences in oxidative stress markers and neurotrophins. Oxidative stress and neurotrophins are reported to regulate angiogenesis. This study aims to examine protein and mRNA levels of vascular endothelial growth factor (VEGF) and VEGF receptor 1 (VEGFR1) in four regions [central maternal (CM), central fetal (CF), peripheral maternal (PM), and peripheral fetal (PF)] of the placenta in normotensive control (NC) women (n = 51) and women with preeclampsia (PE) (n = 43) [18 delivered at term (T-PE) and 25 delivered preterm (PT-PE)]. In all groups, CF region reported highest VEGF protein levels compared to all other regions. VEGF mRNA level was higher in CF region as compared to CM region in PE group (p < 0.05). VEGF levels were lower in all regions of PE, T-PE, and PT-PE groups (p < 0.05) as compared to their respective regions in NC group. VEGFR1 levels were lower in CF (p < 0.05) and PF (p < 0.01) regions as compared to CM region only in control. However, VEGFR1 levels were higher in CF (p < 0.05) and PF (p < 0.01) regions of PT-PE group as compared to control. VEGFR1 mRNA level was higher in PM region of PE group and T-PE group (p < 0.05 for both) as compared to control. VEGF levels in the PF region were positively associated with birth weight and placental weight. This study describes placental regional changes in angiogenic factors particularly highlighting increased VEGF in CF region possibly in response to hypoxic conditions prevailing in placenta.
Topics: Adolescent; Adult; Cross-Sectional Studies; Female; Humans; Placenta; Pre-Eclampsia; Pregnancy; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2
PubMed: 28770473
DOI: 10.1007/s11010-017-3121-y -
Twin Research and Human Genetics : the... Jun 2016Twin-to-twin transfusion syndrome (TTTS) and twin anemia polycythemia sequence (TAPS) are complications unique to monochorionic twin pregnancies and their shared... (Review)
Review
Twin-to-twin transfusion syndrome (TTTS) and twin anemia polycythemia sequence (TAPS) are complications unique to monochorionic twin pregnancies and their shared circulation. Both are the result of the transfusion imbalance in the intertwin circulation. TTTS is characterized by an amniotic fluid discordance, whereas in TAPS, there is a severe discordance in hemoglobin levels. The article gives an overview of the typical features of TTTS and TAPS placentas.
Topics: Amniotic Fluid; Anemia; Female; Fetofetal Transfusion; Hemoglobins; Humans; Placenta; Polycythemia; Pregnancy; Pregnancy, Twin; Twins, Monozygotic
PubMed: 27098457
DOI: 10.1017/thg.2016.29 -
BioTechniques Dec 2020Syncytin-1 (gene ) has been proposed as a marker of pre-eclampsia and malfunctions in placental development. Placenta is heterogeneous tissue, hence the method of biopsy...
Syncytin-1 (gene ) has been proposed as a marker of pre-eclampsia and malfunctions in placental development. Placenta is heterogeneous tissue, hence the method of biopsy can significantly affect the outcome of analyses. A total of 44 placentae were analyzed by taking 3-30 samples from each. Relative levels of expression in the placental biopsies were characterized by RT-qPCR. Evaluation of ten biopsies from one placenta individually (not pooling them) is recommended due to the high variability of expression. No significant correlation was found between biopsy localization and level of expression; therefore, random sampling is recommended. A long cut from the umbilical cord to the edge of the placenta is a convenient approach to placental sampling.
Topics: Adult; Biopsy; Confidence Intervals; Female; Gene Expression Regulation; Gene Products, env; Humans; Placenta; Pregnancy; Pregnancy Proteins; RNA; Specimen Handling
PubMed: 32967447
DOI: 10.2144/btn-2020-0121 -
Hypertension (Dallas, Tex. : 1979) Mar 2019Preeclampsia is one of the leading causes of maternal and neonatal mortality and morbidity worldwide. We have previously reported that magnesium sulfate therapy is...
Preeclampsia is one of the leading causes of maternal and neonatal mortality and morbidity worldwide. We have previously reported that magnesium sulfate therapy is effective for early-onset (EO) preeclampsia. To investigate the molecular mechanisms underlying this favorable effect, metabolomics analysis of magnesium sulfate-treated preeclamptic placentas was performed using capillary electrophoresis time of flight mass spectrometry. There were significant metabolic differences between EO-preeclamptic placentas (n=7) and other placentas (late-onset preeclampsia [n=3], normal pregnancies [n=10]). In EO-preeclamptic placentas, the glutathione metabolism pathway was markedly upregulated, whereas single-sample gene-set enrichment analysis using a publicly available microarray dataset (GSE75010) showed that the glutathione metabolism pathway was significantly downregulated in EO-preeclamptic placentas compared with nonpreeclamptic controls. Metabolomic profiles showed that magnesium sulfate significantly promoted glutathione production in an immortalized trophoblast cell line under oxidative stress conditions but not under normal conditions. Magnesium sulfate suppressed hydrogen peroxide-induced production of reactive oxygen species. Exploratory analysis revealed that urinary 8-isoprostane was decreased in all 5 women treated with magnesium sulfate for preeclampsia with severe features. These findings suggest that magnesium sulfate is effective for treating EO-preeclampsia partly because of its antioxidant effects on trophoblasts.
Topics: Adult; Cell Line; Female; Gestational Age; Glutathione; Humans; Metabolomics; Oxidative Stress; Placenta; Pre-Eclampsia; Pregnancy
PubMed: 30595122
DOI: 10.1161/HYPERTENSIONAHA.118.12389