Placenta最新文献

{"title":"Preeclampsia and transport of ions and small molecules: A literature review","authors":"","doi":"10.1016/j.placenta.2024.09.009","DOIUrl":"10.1016/j.placenta.2024.09.009","url":null,"abstract":"<div><p>Preeclampsia (PE) is a prevalent obstetric complication affecting approximately 3–5% of pregnancies worldwide and is a major cause of maternal and perinatal morbidity and mortality. Preeclampsia is considered a disease of the endothelial system that can progress to eclampsia, characterized by seizures. Early diagnosis and appropriate management are crucial to improving maternal and fetal outcomes, as preeclampsia can lead to severe complications such as placental abruption, fetal growth restriction, and stroke. The pathophysiology of PE is complex, involving a combination of genetic, acquired, and immunological factors. A central feature of the condition is inadequate placentation and impaired uteroplacental perfusion, leading to local hypoxia, endothelial dysfunction, vasoconstriction, and immunological dysregulation. Recent evidence suggests that dysregulation of ion transporters may play a significant role in the adaptation of uterine circulation during placentation. These transporters are essential for maintaining maternal-fetal homeostasis, influencing processes such as nutrient exchange, hormone synthesis, trophoblast cell migration, and the function of smooth muscle cells in blood vessels. In preeclampsia, adverse conditions like hypoxia and oxidative stress result in the downregulation of ion, solute, and water transporters, impairing their function. This review focuses on membrane transporters involved in PE, discussing functional alterations and their physiological implications. The goal of this investigation is to enhance understanding of how dysregulation of ion and small molecule transporters contributes to the development and progression of preeclampsia, underscoring the importance of exploring these signaling pathways for potential therapeutic interventions.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142238440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three transposable elements exhibiting differential expression in pre-eclampsia overlap with enhancer regions","authors":"","doi":"10.1016/j.placenta.2024.09.010","DOIUrl":"10.1016/j.placenta.2024.09.010","url":null,"abstract":"<div><div>Transposable elements (TEs) play a crucial role in placental development and dysfunction. Our study examined TE expression in pre-eclampsia (PE) using RNA-seq datasets. We identified differentially expressed TEs and explored the genomic location of the most significant TEs, investigating their possible regulatory roles. Notably, three TEs overlapped with putative enhancer regions, suggesting a potential regulatory impact on gene expression. These findings highlight the regulatory potential of TEs and their importance in placental development, supporting that TE dysregulation may contribute to PE pathogenesis.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143400424006532/pdfft?md5=049757458aa2caa4a0cff5d23dc9a36d&pid=1-s2.0-S0143400424006532-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of Urotensin II expression in placenta and umbilical cord in pregnancies with intrauterine growth restriction by histological and biochemical methods","authors":"","doi":"10.1016/j.placenta.2024.09.003","DOIUrl":"10.1016/j.placenta.2024.09.003","url":null,"abstract":"<div><h3>Objective</h3><p>In this study, it was aimed to investigate Urotensin II in intrauterine growth restriction (IUGR) and its connection to autophagy and/or apoptosis in placenta and umbilical cord by immunohistochemical and biochemical methods.</p></div><div><h3>Materials and methods</h3><p>The study included 30 healthy pregnant women and 30 pregnant women with IUGR, aged 19–45, at Atatürk University Gynecology Clinic. Samples were collected from placenta, umbilical cord, maternal blood, and umbilical cord blood during delivery. Histopathological examination was carried out on placenta and umbilical cord, and UTII, Beclin 1, and caspase 3 expressions were analyzed in these tissues. Biochemical analysis was performed on maternal and umbilical cord serum samples.</p></div><div><h3>Results</h3><p>In healthy placentas, normal villus formation was seen, but those with IUGR showed accelerated villus maturation, causing inadequate nutrition and development. IUGR placentas had fibrin deposition, villous edema, syncytial nodes increase, and intervillous distance. Umbilical cords of IUGR group had differences in vessel wall thickness, arterial lumens, and vessel number. Higher levels of UTII, Beclin 1, and caspase 3 were found in IUGR placenta and cord. Beclin 1 and caspase 3 levels were significantly higher in IUGR group compared to controls, while UTII levels were not significantly different in maternal and cord serums.</p></div><div><h3>Conclusion</h3><p>As a result of our findings, UTII increase in placenta and umbilical cord may lead to IUGR formation by inducing autophagy and apoptosis.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142271465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial dysfunction and oxidative stress in selective fetal growth restriction","authors":"","doi":"10.1016/j.placenta.2024.09.005","DOIUrl":"10.1016/j.placenta.2024.09.005","url":null,"abstract":"<div><h3>Introduction</h3><p>Placental dysfunction is the primary cause of selective fetal growth restriction (sFGR), and the specific role of mitochondria remains unclear. This study aims to elucidate mitochondrial functional defects in sFGR placentas and explore the roles of mitochondrial genomic and epigenetic alterations in its pathogenesis.</p></div><div><h3>Methods</h3><p>The placental villi of MCDA twins with sFGR were collected and the morphology and number of mitochondria were observed by transmission electron microscopy. Meanwhile, the levels of reactive oxygen species (ROS), ATP and oxidative damage markers were assessed. Mitochondrial DNA (mtDNA) copy number detection, targeted sequencing and methylation sequencing were performed. The expression of placental cytochrome c oxidase subunit I (COX I) and mitochondrial long non-coding RNAs (lncRNAs) were evaluated by Western blotting and qPCR.</p></div><div><h3>Results</h3><p>Compared with placentae from normal fetuses, pronounced mitochondrial damage within cytotrophoblast was revealed in sFGR placentae, alongside augmented mitochondrial number in syncytiotrophoblast. Enhanced oxidative stress in these placentae was evidenced by elevated markers of oxidative damage, accompanied by increased ROS production and diminished ATP generation. In sFGR placentae, a notable rise in mitochondrial copy number and one heterozygous mutation in the <em>MT-RNR2</em> gene were observed, along with decreased COX Ⅰ levels, increased lncND5, lncND6, lncCyt b, and MDL1 synthesis, and decreased RMRP synthesis.</p></div><div><h3>Discussion</h3><p>Findings collectively confirmed an exacerbation of oxidative stress within sFGR placentae, coinciding with mitochondrial dysfunction, compromised energy production, and ultimately the failure of compensatory mechanisms to restore energy balance, which may result from mutations in the mitochondrial genome and abnormal expression of epigenetic regulatory genes.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142168210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single vs. multi-slice assessments of in vivo placental T2∗ measurements","authors":"","doi":"10.1016/j.placenta.2024.09.006","DOIUrl":"10.1016/j.placenta.2024.09.006","url":null,"abstract":"<div><h3>Introduction</h3><p>Placental health is vital for maternal and fetal well-being, and placental T2∗ has been suggested to identify in vivo placental dysfunction prior to delivery. However, ideal regions of interest to best inform functional assessments of the placenta remain unknown. The aim of this study is to compare global and slice-wise measures of in-vivo placental T2∗ assessments.</p></div><div><h3>Methods</h3><p>This prospective study recruited pregnant people with singleton pregnancies between December 2017 and February 2022.3D multi-echo RF-spoiled gradient echo sequences were acquired, and placental T2∗ values were derived from global and slice-wise approaches. Statistical analyses included Pearson correlation coefficients, concordance correlation coefficients (CCC), intraclass correlation coefficients (ICC), and Bland-Altman analyses.</p></div><div><h3>Results</h3><p>Of 115 participants (mean gestational age, 29.25 ± 5.05 weeks), 68 were healthy controls, and 47 were high-risk pregnancies. Global and slice-wise placental T2∗ assessments for the entire cohort showed no significant difference nor for individual subgroups (healthy controls or high-risk). Pearson correlation values ranged between 0.88 and 0.99 for mean global and slice-wise placental T2∗. CCC analyses ranged from 0.88 to 0.99 for mean T2∗, and ICC analyses ranged between 0.88 and 0.99 for mean T2∗, showing a strong agreement between measurements. Bland-Altman analyses depicted T2∗ differences across coverage methods, and groups resided within the 95 % limits of agreement.</p></div><div><h3>Discussion</h3><p>Single-slice placental assessments offer robust, comparable T2∗ values to global assessments, with the added benefit of reducing post-processing time and SAR exposure. This supports slice-wise approaches as valid alternatives for assessing placental health in various pregnancies.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142238563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa-miR-3928–3p targets the CCL3/CCR5 axis to induce amniotic epithelial cell senescence involved in labor initiation","authors":"","doi":"10.1016/j.placenta.2024.09.008","DOIUrl":"10.1016/j.placenta.2024.09.008","url":null,"abstract":"<div><h3>Introduction</h3><p>Senescence in human amniotic epithelial cells (hAECs) and increased sterile inflammation in the amniotic cavity can lead to the initiation of term labor (TL). We investigated the possible roles of hsa-miR-3928–3p and chemokine ligand 3 (CCL3) in labor initiation and the underlying molecular mechanisms.</p></div><div><h3>Methods</h3><p>Microarray chip screening was used to analyse the differential expression of miRNAs in amniotic fluid exosomes from women in TL and term not-in-labor. The GEO and miRWalk databases were used to identify differential genes, and a dual luciferase assay was used to verify the relationship. Reverse transcription quantitative PCR (RT-qPCR) and immunofluorescence were used to determine the expression and localization of CCL3/CCR5 in fetal membranes. RT-qPCR and western blotting were used to detect the expression of <em>CCL3/CCR5</em> in hAECs with hsa-miR-3928–3p knockdown/overexpression. Cell counting kit 8, flow cytometry, EdU proliferation, senescence-associated β-galactosidase, and enzyme-linked immunosorbent assays were performed to detect the impact of hsa-miR-3928–3p on hAEC function.</p></div><div><h3>Results</h3><p>hsa-miR-3928–3p expression was downregulated in TL. <em>CCL3</em> (macrophage inflammatory protein-1α) was identified as a differentially expressed target gene. hsa-miR-3928–3p targeted the 3′ UTR of <em>CCL3</em>. Downregulation of hsa-miR-3928–3p expression increased <em>CCL3</em> expression. CCL3, via its CCR5 receptor, decreased the proliferation, but increased the senescence, apoptosis rate, secretion of inflammatory factors (IL-8, TNF-α, and IL-6), and expression of senescence-associated protein p21 in hAECs.</p></div><div><h3>Discussion</h3><p>hsa-miR-3928–3p negatively regulates <em>CCL3</em>, promoting hAEC senescence through the CCL3-CCR5 axis and inducing signals for labor initiation. These findings provide novel insights for labor initiation in clinical settings.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142238564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Down-regulation of CORO1C mediated by lncMALAT1/miR-133a-3p axis contributes to trophoblast dysfunction and preeclampsia","authors":"","doi":"10.1016/j.placenta.2024.09.007","DOIUrl":"10.1016/j.placenta.2024.09.007","url":null,"abstract":"<div><h3>Introduction</h3><p>Placental trophoblast dysfunction has been proved to be closely related to the pathogenesis of preeclampsia. Coronaryxin-like actin-binding protein 1C (CORO1C) plays an important role in cell proliferation, apoptosis, invasion, and signal transduction, but its involvement in trophoblast dysfunction and preeclampsia remains uncertain.</p></div><div><h3>Methods</h3><p>The expression of CORO1C in placental tissues of preeclampsia (PE) pregnant women and pregnant mice PE model were detected by real-time quantitative polymerase chain reaction (RT-qPCR), western blotting (WB) and immunohistochemical (IHC) staining. Next, the proliferation, invasion, migration and apoptosis were performed to explore the functions of CORO1C in HTR8/SVneo cell. Furthermore, the expression of CORO1C were detected in lncMALAT1 knockdown and overexpression HTR-8/SVneo cell. And then we investigated the possible regulatory mechanism of lncMALAT1 on CORO1C through bioinformatics analysis, FISH assays, RIP assays, RNA pull down and dual luciferase reporter assays. Finally, we further validated that lncMALAT1 regulate the function of placental trophoblast cells through CORO1C.</p></div><div><h3>Results</h3><p>The expression of CORO1C was significantly decreased in the placenta of PE patients and mice model, and positively associated with neonatal birth weight. And we found that CORO1C inhibited trophoblast proliferation, migration and invasion. Furthermore, reduced expression of lncMALAT1 impaired CORO1C level, thereby resulting in trophoblast dysfunction. Mechanistically, the dysregulation of lncMALAT1 promoted the expression of miR-133a-3p, strongly enhancing its binding to the 3′UTR region of CORO1C mRNA for degradation.</p></div><div><h3>Discussion</h3><p>This study demonstrated that the dysregulation of CORO1C via lncMALAT1/miR-133a-3p axis impairs trophoblast function and contributes to preeclampsia pathogenesis, providing novel insights in PE therapy through modulating CORO1C level.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143400424006507/pdfft?md5=8805885d56cfd181cde6066cffde999f&pid=1-s2.0-S0143400424006507-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142232555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trophoblast Research Editorial 27th International Federation of Placenta Associations Conference, Rotorua, New Zealand","authors":"Larry Chamley","doi":"10.1016/j.placenta.2024.09.004","DOIUrl":"https://doi.org/10.1016/j.placenta.2024.09.004","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142257787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF6 negatively regulates HIF-1α in extravillous trophoblasts under hypoxia","authors":"","doi":"10.1016/j.placenta.2024.09.002","DOIUrl":"10.1016/j.placenta.2024.09.002","url":null,"abstract":"<div><h3>Introduction</h3><p>HIF-1α, the master regulator of hypoxia cellular response, is stabilized under low oxygen levels and degraded in the presence of oxygen but its transcription, translation, and degradation are tightly regulated by numerous pathways. KLF6 is a transcription factor involved in proliferation, differentiation, and apoptosis in several cell systems. Under hypoxia it is upregulated in a HIF-1α-dependent manner in extravillous trophoblasts. Considering the importance of hypoxia modulation of EVT behavior through HIF1-α we aimed to study whether KLF6 modulates HIF-1α expression in HTR8/SVneo cells.</p></div><div><h3>Methods</h3><p>HTR8/SVneo cells were cultured in a 1 % oxygen chamber or in 3D format where a spontaneous oxygen gradient is generated. qRT-PCR and Western blot were performed to analyze mRNA and protein expression, respectively. SiRNA, shRNA, or plasmids were used to down- or up-regulate gene expression. Wound healing assay was performed under hypoxia to evaluate migration. The NFκB pathway was modulated with dominant negative mutants and a chemical inhibitor. Cobalt chloride was used to block HIF-1α degradation.</p></div><div><h3>Results</h3><p>KLF6 up- and down-regulation in HTR8/SVneo cells exposed to acute hypoxia revealed a negative regulation on HIF-1α. KLF6 silencing led to a partially HIF-1α-dependent increase in MMP9 and VEGF. The NF-κB pathway and HIF-1α degradation were involved in KLF6-dependent HIF-1α regulation. HTR8/SVneo-3D culture showed that KLF6 negatively regulates HIF-1α in a microenvironment with naturally generated hypoxia.</p></div><div><h3>Discussion</h3><p>Present results reveal that KLF6 contributes to a fine tune modulation of HIF-1α level under hypoxia. Thus, sustaining a HIF-1α homeostatic level, KLF6 might contribute to control EVT adaptation to hypoxia.</p></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142148474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A straightforward cell culture insert model to incorporate biochemical and biophysical stromal properties into transplacental transport studies","authors":"Katherine M. Nelson, Bryan J. Ferrick, Hassan Karimi, Christine L. Hatem, Jason P. Gleghorn","doi":"10.1016/j.placenta.2024.09.001","DOIUrl":"https://doi.org/10.1016/j.placenta.2024.09.001","url":null,"abstract":"The placental extracellular matrix (ECM) dynamically remodels over pregnancy and in disease. How these changes impact placental barrier function is poorly understood as there are limited models of the placenta with a modifiable stromal compartment to mechanistically investigate these extracellular factors. We developed a straightforward method to incorporate uniform hydrogels into standard cell culture inserts for transplacental transport studies. Uniform polyacrylamide (PAA) gels were polymerized within cell culture inserts by (re)using the insert packaging to create a closed, controllable environmental chamber. PAA pre-polymer solution was added dropwise via a syringe to the cell culture insert and the atmosphere was purged with an inert gas. Transport and cell culture studies were conducted to validate the model. We successfully incorporated ECM-functionalized uniform PAA gels into cell culture inserts, enabling cell adhesion and monolayer formation. Imaging and analyte transport studies validated gel formation and expected mass transport results, and successful cell studies confirmed cell viability, stiffness-mediated YAP translocation, and that the model could be used in transplacental transport studies. Detailed methods and validation protocols are included. The incorporation of a PAA gel within a cell culture insert enables independent study of placental ECM biophysical and biochemical properties in the context of transplacental transport. These straightforward and low-cost methods to build three-dimensional cellular models are readily adoptable by the wider scientific community.","PeriodicalId":20203,"journal":{"name":"Placenta","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142257786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}