Placenta最新文献

{"title":"Gene regulation and intercellular communication at single cell level in placentas from women with polycystic ovary syndrome treated with metformin during pregnancy","authors":"Hong Jiang , Emilie Derisoud , Denise Parreira , Paulo R. Jannig , Eszter Vanky , Elisabet Stener-Victorin , Qiaolin Deng","doi":"10.1016/j.placenta.2024.10.036","DOIUrl":"10.1016/j.placenta.2024.10.036","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 147"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143376875","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 novel microarray analyzer for prediction of preeclampsia using multi surface biomarkers on placental extracellular vesicle from maternal plasma","authors":"Marei Sammar , Malene Møller Jørgensen , Rikke Bæk , Hamutal Meiri","doi":"10.1016/j.placenta.2024.10.037","DOIUrl":"10.1016/j.placenta.2024.10.037","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 147-148"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143376876","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":"3D quantification analysis of the microvillous membrane of the human placental syncytiotrophoblast","authors":"Ella Proudley , Davis Laundon , Jane Cleal , Rohan Lewis","doi":"10.1016/j.placenta.2024.10.057","DOIUrl":"10.1016/j.placenta.2024.10.057","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 154"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377517","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":"Impact of feto-placental small extracellular vesicles on preeclampsia and fetal immunity","authors":"Michaela Stoiber , Birgit Hirschmugl , Carolina Kauer , Barbara Darnhofer , Katharina Eberhard , Harald Köfeler , Karl Kashofer , Christian Wadsack","doi":"10.1016/j.placenta.2024.10.038","DOIUrl":"10.1016/j.placenta.2024.10.038","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 148"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377681","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":"Dual effects of arachidonic acid and Piezo1 on feto-placental endothelial barrier function","authors":"Nilüfer Kamali Simsek , Monika Horvat Merčnik , Christian Wadsack , Hanna Allerkamp","doi":"10.1016/j.placenta.2024.10.044","DOIUrl":"10.1016/j.placenta.2024.10.044","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 150"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377863","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":"Arsenic and the placenta: A review with emphasis on the immune system","authors":"Kristal A. Rychlik ,&nbsp;Emily J. Illingworth ,&nbsp;Fenna C.M. Sillé","doi":"10.1016/j.placenta.2024.12.019","DOIUrl":"10.1016/j.placenta.2024.12.019","url":null,"abstract":"<div><div>Chronic arsenic exposure affects over 140 million people globally. While arsenic easily crosses the placenta, the specific mechanisms impacting placental immune cell populations and fetal health are unclear. Maternal arsenic exposure is epidemiologically linked to increased infection risk, mortality, and cancer susceptibility in offspring, emphasizing the importance of understanding placentally-mediated immune effects. This review explores the potential role of the placenta, a key organ for immune transfer to the developing fetus, in mediating chronic low-dose arsenic exposure effects.</div><div>Examining three potential pathways—direct contaminant transfer, altered immune transfer from the mother, and indirect impact on fetal immune programming via maternal and placental signaling—the review highlights studies associating maternal arsenic levels with immune-related outcomes, including changes in cord blood T cell populations and increased placental inflammation. Placental gene expression analysis reveals alterations in pathways related to oxidative stress, proteasome activity, and aquaglyceroporin transporter expression. Impact on placental DNA methylation and microRNA regulation as well as on trophoblast dysfunction is discussed, with evidence suggesting inhibited trophoblast migration and placental growth factor expression. The complexity of mixtures, nutrition, and environmental interactions add challenges to investigating the placenta's role in immune programming.</div><div>Despite inconsistent findings on placental morphology alterations, evidence suggests a potential link between arsenic exposure, placental anomalies, and adverse birth outcomes. Further research is crucial to comprehend the effects of prenatal arsenic exposure on trophoblasts, placental immune cells, and subsequent long-term consequences for fetal immune development and birth outcomes.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 73-81"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953774","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":"The maternal body mass index and first-trimester placental (vascular) development","authors":"Nicole Schenkelaars ,&nbsp;Sam Schoenmakers ,&nbsp;Marijke M. Faas ,&nbsp;Sten P. Willemsen ,&nbsp;Eline S. de Vos ,&nbsp;Régine P.M. Steegers-Theunissen","doi":"10.1016/j.placenta.2024.12.015","DOIUrl":"10.1016/j.placenta.2024.12.015","url":null,"abstract":"<div><h3>Background</h3><div>Maternal obesity is associated with maternal complications, including hypertensive disorders of pregnancy (HDP), and related fetal complications, such as fetal growth restriction. During pregnancy, the placenta is one of the key regulators of embryonic and fetal growth. Previous studies mainly investigated placental growth by measuring postpartum placental weight. However, the effects of obesity on aberrant placental and fetal growth might occur already in the first trimester.</div></div><div><h3>Objectives</h3><div>Investigate associations between maternal BMI and first-trimester features of placental size and vascular development.</div></div><div><h3>Study design</h3><div>870 women were included from a prospective cohort study. BMI was measured &lt;10 weeks of gestation. Transvaginal 3D Power Doppler ultrasounds were obtained at 7, 9, and 11 weeks of gestation to measure placental volume (PV) and utero-placental vascular volume (uPVV). Associations between BMI and utero-placental (vascular) volume trajectories were assessed using mixed models, adjusted for covariates.</div></div><div><h3>Results</h3><div>Associations were found between maternal BMI and PV (non-linear model; <em>p</em> = 0.022). A BMI ≥34 kg/m² showed decreased first-trimester PV compared to normal weight (Δ∛PV=−0.070, 95%CI -0.136 to −0.004, <em>p</em>=0.039). Negative associations were found between maternal BMI and uPVV (β=−0.027, 95%CI -0.041 to −0.014, <em>p</em>&lt;0.001). Exclusion of women developing HDP, attenuated the association with PV (non-linear model; <em>p</em>=0.152), whilst the association between uPVV remained (β=−0.031, 95%CI -0.046 to −0.016, <em>p</em>=0.001).</div></div><div><h3>Conclusion</h3><div>Increased maternal BMI is associated with decreasing first-trimester uPVV, moreover, in women with a BMI ≥34 kg/m² the PV is decreased. These findings suggest tissue-specific changes in the placental development of women with obesity.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 126-134"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142966331","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":"The overview of lactylation in the placenta of preeclampsia","authors":"Qiaoli Feng ,&nbsp;Ping Yang ,&nbsp;Jinli Lyu ,&nbsp;Xinyang Liu ,&nbsp;Shilin Zhong ,&nbsp;Yiheng Liang ,&nbsp;Ping Liu ,&nbsp;Liting Huang ,&nbsp;Shangrong Fan ,&nbsp;Xiaowei Zhang","doi":"10.1016/j.placenta.2025.01.003","DOIUrl":"10.1016/j.placenta.2025.01.003","url":null,"abstract":"<div><h3>Background</h3><div>Preeclampsia is a major challenge for obstetricians due to its severe impacts on maternal and fetal health. Lysine lactylation (Kla) derived from lactate is a novel type of post-translational modification which has been confirmed to affect the malignant progression of diseases as an epigenetic modifier. However, the systemic lactylome profiling of preeclampsia is still unclear.</div></div><div><h3>Material and methods</h3><div>Immunohistochemistry and protein immunoassay were performed on placenta tissues from preeclamptic patients and control pregnancies to compare lactylation levels between the groups. Then liquid chromatography-tandem mass spectrometry (LC-MS/MS) was utilized for quantitative lactylomic analysis and proteomic assessment for proteins with differentially lactated modification. Bioinformatics analyses were applied to reveal the conserved motif sequences and enrichment pathways.</div></div><div><h3>Results</h3><div>Significant differences in protein lactylation levels were evident in the placenta between preeclamptic and control groups, with modifications observed in both histone and non-histone proteins. Lactylome analysis showed significant downregulation of 59 Kla proteins and 69 Kla sites in preeclamptic placentas, whereas 44 proteins and 60 sites were upregulated. These differentially lactylated proteins were primarily mitochondrial and associated with the citrate cycle (TCA cycle). Enriched metabolic pathways linked to lactylation included those important for vascular muscle contraction, platelet activation, and several signaling pathways like PI3K-Akt, PPAR, and cholesterol metabolism.</div></div><div><h3>Conclusions</h3><div>Preeclamptic placentas exhibit distinct lactylation profiles compared to normal pregnancies, primarily affecting mitochondrial and TCA cycle-related energy metabolism. These changes contribute to the pathophysiology of preeclampsia by involving metabolic pathways critical for angiogenesis and endothelial function.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 135-143"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971926","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":"Priority Setting Partnership on Placental Pathology: Consensus recommendations for placental research","authors":"Mauritia C. Marijnen ,&nbsp;M.I. Bügel ,&nbsp;T. Yee Khong ,&nbsp;Neil J. Sebire ,&nbsp;Alexander E.P. Heazell ,&nbsp;Wessel Ganzevoort ,&nbsp;Frank H. Bloomfield ,&nbsp;Elisabeth M.W. Kooi ,&nbsp;Lotte-Elisabeth van der Meeren ,&nbsp;Sanne J. Gordijn","doi":"10.1016/j.placenta.2024.12.020","DOIUrl":"10.1016/j.placenta.2024.12.020","url":null,"abstract":"<div><h3>Introduction</h3><div>The placenta supports the metabolic and respiratory requirements of the fetus. Placental disorders, caused by various pathophysiological mechanisms, may result in adverse pregnancy and neonatal outcomes. Knowledge gaps remain in the understanding, reporting and interpretation of placental pathology relating to clinical conditions. This project aimed to collaboratively identify the most important unanswered research questions related to placental pathology.</div></div><div><h3>Methods</h3><div>An international Priority Setting Partnership (PSP) was conducted, involving (perinatal) pathologists, obstetricians, paediatrician-neonatologists, midwives, and scientists with expertise in placental pathology. In the first survey, participants identified their three most important unanswered research questions. Afterwards literature was reviewed for evidence on the proposed questions. In a second survey, participants ranked the most important questions from an initial long-list. The top-ranked questions were then discussed and finalized in a 1-h online consensus workshop.</div></div><div><h3>Results</h3><div>Ninety participants completed the first survey. The majority of stakeholders were perinatal pathologists (n = 39 (43.3 %) and most were based in Europe (n = 43 (47.8 %). 270 questions were submitted; after review, these were subdivided into 32 overarching questions. The second ranking survey was completed by 53 participants. Twenty-five participants attended the online workshop, which reached consensus on the top 10. The questions focus, among others, on causes, recurrence risk, consistency of reporting, diagnosing tools and potential use of artificial intelligence.</div></div><div><h3>Discussion</h3><div>Following this international PSP, the top 10 prioritized research questions on placental pathology have been identified. This will inform the research agenda for funders and policy-makers, and is intended to improve care for patients suffering from placental insufficiency.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 67-72"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953776","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":"Profiling epithelial viral receptor expression in amniotic membrane and nasal epithelial cells at birth","authors":"Bailee Renouf ,&nbsp;Erika N. Sutanto ,&nbsp;Courtney Kidd ,&nbsp;James Lim ,&nbsp;Minda Amin ,&nbsp;Luke Berry ,&nbsp;Gerard F. Hoyne ,&nbsp;Nina D'Vaz ,&nbsp;Elizabeth Kicic-Starcevich ,&nbsp;Stephen M. Stick ,&nbsp;Thomas Iosifidis ,&nbsp;the AERIAL study team","doi":"10.1016/j.placenta.2024.12.029","DOIUrl":"10.1016/j.placenta.2024.12.029","url":null,"abstract":"<div><h3>Introduction</h3><div>Children with wheeze and asthma present with airway epithelial vulnerabilities, such as impaired responses to viral infection. It is postulated that the <em>in utero</em> environment may contribute to the development of airway epithelial vulnerabilities. The aims of the study were to establish whether the receptors for rhinovirus (RV), respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are expressed in the amniotic membrane and whether the pattern of expression is similar to newborn nasal epithelium.</div></div><div><h3>Methods</h3><div>Placenta were collected (n = 33) from newborns in AERIAL, a sub-study nested under the ORIGINS birth cohort. Using purified RNA from amniotic samples (n = 33), along with previously extracted RNA from nasal epithelial cells from newborns (n = 20), real-time quantitative polymerase chain reaction (qPCR) was performed to determine gene expression of viral receptors for RV, RSV and SARS-CoV-2 in both amniotic and newborn nasal epithelial samples. In addition, receptor protein expression was quantified through Western blot and localised using immunohistochemical staining in amniotic samples.</div></div><div><h3>Results</h3><div>Amniotic and newborn nasal samples expressed various receptors for RV (<em>ICAM-1, LDLR, CDHR3</em>), RSV (<em>NCL, CX3CR1</em>) and SARS-CoV-2 (<em>ACE2, TMPRSS2</em>) at the gene level, although the magnitude of expression varied. In addition, protein expression of these receptors was confirmed in the amniotic samples. These proteins were localised to the epithelial layer of the amniotic membrane.</div></div><div><h3>Conclusion</h3><div>This proof-of-concept study indicates the potential of amniotic samples to facilitate investigation into the interactions between the <em>in utero</em> environment and prenatal programming of epithelial innate immune responses to viruses.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 82-88"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953778","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}