Placenta最新文献

{"title":"Down-regulation of TAGLN2 associated with the development of preeclampsia by effecting the Rap1 signaling pathway","authors":"Ping Yang ,&nbsp;Xinyang Liu ,&nbsp;Jinli Lyu ,&nbsp;Qiaoli Feng ,&nbsp;Yuzhen Ding ,&nbsp;Shilin Zhong ,&nbsp;Ping Liu ,&nbsp;Yiheng Liang ,&nbsp;Chunfeng Liu ,&nbsp;Liting Huang ,&nbsp;Pingyue Zhao ,&nbsp;Qing Li ,&nbsp;Kaidong Ma ,&nbsp;Shangrong Fan ,&nbsp;Xiaowei Zhang","doi":"10.1016/j.placenta.2024.11.009","DOIUrl":"10.1016/j.placenta.2024.11.009","url":null,"abstract":"<div><h3>Introduction</h3><div>Preeclampsia (PE) poses significant global challenges to pregnancy health, being a leading cause of maternal and perinatal morbidity and mortality. Unfortunately, effective treatment options remain limited, necessitating the urgent development of novel therapeutic strategies. This study is to investigate down-regulation of Transgelin-2 (TAGLN2) contributes to the development of PE through suppression of the Rap1 signaling pathway.</div></div><div><h3>Methods</h3><div>Placentas from PE patients were collected for a transcriptome analysis. Down-regulation experiments of TAGLN2 were performed in mouse and HTR-8/SVneo cells to generate PE models. The mechanism by which down-regulation of TAGLN2 induces PE was explored based on these PE model through transcriptome and proteome analysis and molecular tests.</div></div><div><h3>Results</h3><div>Our findings revealed that the expression levels of Rap1A was significantly reduced in the placenta of PE patients. The expression level of Rap1A in the placental tissue of sh_Tagln2 PE model mice is down-regulated. In addition, TAGLN2 down-regulation impede the proliferation and migration of HTR8/SVneo cells and lead to the decreased expression of Rap1A. Meanwhile, Rap1A down-regulation impede both the proliferation and migration of HTR8/SVneo cells. Both transcriptomic and proteomic levels of sh-TG2 HTR8/Svneo cells demonstrated Rap1 signaling pathway and related key genes was inhibited after TAGLN2 down-regulation.</div></div><div><h3>Conclusion</h3><div>Our results confirm that down-regulation of TAGLN2 in HTR-8/SVneo cells leads to the decreased Rap1A expression and suppresses trophoblast cell proliferation and migration by inhibiting Rap1 signaling pathway. Meanwhile, Rap1A down-regulation impede both the proliferation and migration of HTR8/SVneo cells. These findings concluded that down-regulation of TAGLN2 may be implicated in the development of preeclampsia through its effect on the Rap1 signaling pathway.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"159 ","pages":"Pages 20-31"},"PeriodicalIF":3.0,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142740149","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":"Lower level of miR-34a leads to placenta accreta spectrum by promoting the proliferation, migration of trophoblast villous epithelial cells and enhanced the angiogenesis of vascular endothelial cells","authors":"Te-Yao Hsu ,&nbsp;Chih-Chang Tsai ,&nbsp;Hsin-Hsin Cheng ,&nbsp;Kuo-Chung Lan ,&nbsp;Hsuan-Ning Hung ,&nbsp;Wan-Ting Huang ,&nbsp;Yun-Ju Lai ,&nbsp;Kun-Long Huang ,&nbsp;Huey-Ling You ,&nbsp;Ping-Chung Tsai ,&nbsp;Chia-Ing Jan ,&nbsp;Sung-Chou Li","doi":"10.1016/j.placenta.2024.11.012","DOIUrl":"10.1016/j.placenta.2024.11.012","url":null,"abstract":"<div><h3>Introduction</h3><div>The overall prevalence of placenta accreta spectrum (PAS) is approximately 0.17 %, but it accounts for 7 % of maternal mortality and is associated with intraoperative and postoperative morbidity. The pathogenesis mechanisms of PAS include an imbalance between decidualization and trophoblast invasion. The aim of this study is to identify the pathogenesis roles of miR-34a in PAS.</div></div><div><h3>Methods</h3><div>For this purpose, we collected 15 placenta tissues from pregnant subjects with PAS complications and another 15 placenta tissues from normal pregnancy (NP) cases. Then, we conducted <em>in situ</em> hybridization assay to compare miR-34a expression level, followed by <em>in vitro</em> simulations of NP and PAS with miR-34a and scrambled control (SC) mimic transfection in cells, respectively. Next, we conducted <em>in vitro</em> cellular assays to investigate the pathogenesis mechanisms of miR-34a in PAS.</div></div><div><h3>Results</h3><div>We first confirmed significantly lower level of miR-34a in the trophoblast villous (TV) from PAS patients. By <em>in vitro</em> assays, lower miR-34a led to significantly higher cell proliferation and enhanced cell migration in TV epithelial cells. In addition, lower miR-34a resulted in elevated angiogenesis ability in vascular endothelial cells. Finally, to identify the pathway involved by miR-34a in PAS, we used microarray (raw data available via NCBI GEO database with accession number <span><span>GSE279257</span><svg><path></path></svg></span>) and flow cytometry to confirm that lower miR-34a significantly repressed the apoptosis activity in TV epithelial cells.</div></div><div><h3>Discussion</h3><div>In this study, we not only confirmed miR-34a as a biomarker of PAS but also clarified the <em>in vitro</em> pathogenesis mechanism of miR-34a in PAS.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"159 ","pages":"Pages 1-8"},"PeriodicalIF":3.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142740245","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":"Aberrant expression of solute carrier family transporters in placentas associated with pregnancy complications","authors":"Swati Ajmeriya ,&nbsp;Neha Kashyap ,&nbsp;Anamta Gul ,&nbsp;Ashok Ahirwar ,&nbsp;Sunil Singh ,&nbsp;Smita Tripathi ,&nbsp;Ruby Dhar ,&nbsp;Nihar R. Nayak ,&nbsp;Subhradip Karmakar","doi":"10.1016/j.placenta.2024.11.011","DOIUrl":"10.1016/j.placenta.2024.11.011","url":null,"abstract":"<div><h3>Introduction</h3><div>Solute carrier family transporters (SLCs), crucial for nutrient and trace element uptake in the placenta, play a significant role in fetal growth and development. Their dysregulation is associated with various pregnancy disorders. However, a comprehensive understanding of their role and regulation in placental function and pregnancy complications is still a largely unexplored area, making this study novel and significant.</div></div><div><h3>Methods</h3><div>We performed a rigorous meta-analysis of publicly available NCBI GEO microarray and RNA-Seq datasets followed by bioinformatics analysis of differentially expressed SLCs in PE and IUGR. The identified SLCs were then validated using qPCR on PE placental samples, ensuring the reliability and validity of the findings.</div></div><div><h3>Results</h3><div>Bioinformatics analysis of preeclampsia (PE) and Intrauterine Growth restriction (IUGR) datasets revealed significant associations between specific SLC transporters with disease pathology, identified by studying differentially expressed SLCs. Subsequent validation using qPCR on placental samples confirmed considerable downregulation of SLC6A8, SLC16A10, SLC25A3, and SLC29A3, highlighting their dysregulation in the pathogenesis of PE and IUGR.</div></div><div><h3>Discussion</h3><div>The significant downregulation of SLC6A8, SLC16A10, SLC25A3, and SLC29A3 observed by bioinformatics analyses and validated by qPCR indicates atypical expression of these SLCs in gestational disorders. Our findings underscore the potential contribution of multiple SLC gene families to the development of placental pathologies associated with diverse pregnancy complications.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"159 ","pages":"Pages 9-19"},"PeriodicalIF":3.0,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142740083","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":"Maternal dietary olive oil protects diabetic rat offspring from impaired uterine decidualization.","authors":"Cintia Romina Gatti, Florencia Schibert, Virginia Soledad Taylor, Evangelina Capobianco, Verónica Montero, Romina Higa, Alicia Jawerbaum","doi":"10.1016/j.placenta.2024.11.010","DOIUrl":"https://doi.org/10.1016/j.placenta.2024.11.010","url":null,"abstract":"<p><strong>Introduction: </strong>Maternal diabetes increases the risk of adverse maternal, perinatal and offspring outcomes. This study aimed to address whether alterations in uterine decidualization are programmed in the prepubertal offspring from diabetic rats fed diets enriched or not in extra virgin olive oil (EVOO).</p><p><strong>Methods: </strong>Control and mild pregestational diabetic female rats (F0) were mated with control males and fed diets enriched or not with 6 % EVOO during pregnancy. Offspring (F1) were evaluated on postnatal day 30, after induction of uterine decidualization (PMSG 50 IU- hCG 50 IU). Signaling pathways involved in decidualization, including prolactin, PPAR and mTOR pathways as well as microRNAs (miRs) regulating these pathways were evaluated by Western blot or qPCR in the decidualized uteri.</p><p><strong>Results: </strong>The offspring from diabetic rats evidenced reduced prolactin and prolactin receptor levels in the decidualized uteri. Additionally, these tissues showed increased PPARγ levels and reduced levels of its negative regulators miR-19b and miR-155. MiR-21, a microRNA that targets both PPARα and mTOR pathway regulators was reduced, whereas PPARα, PTEN and FOXO1 mRNA levels were increased in the decidualized uteri of the offspring from diabetic rats. The mTOR pathway activity was reduced in the decidualized uteri of the offspring from diabetic rats. Most of the observed alterations were prevented by the EVOO-enriched maternal diet.</p><p><strong>Discussion: </strong>Impaired pathways relevant to decidualization are programmed in the uteri of prepubertal offspring from diabetic dams, alterations capable of being prevented by maternal diets enriched in EVOO.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751045","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":"Abnormal placental development induced by repeated cesarean sections: Investigating an animal model of placenta accreta spectrum disorders","authors":"Yongdan Ma ,&nbsp;Yongyan Hu ,&nbsp;Jiajun He ,&nbsp;Xin Wen ,&nbsp;Huixia Yang ,&nbsp;Jingmei Ma","doi":"10.1016/j.placenta.2024.11.008","DOIUrl":"10.1016/j.placenta.2024.11.008","url":null,"abstract":"<div><h3>Introduction</h3><div>Placenta accreta spectrum (PAS) is a serious condition associated with severe postpartum hemorrhage, leading to emergency hysterectomy. Research has predominantly focused on clinical diagnosis and the prevention of adverse maternal outcomes, but the underlying pathological mechanisms remain poorly understood, partly due to the limitations of animal models.</div></div><div><h3>Methods</h3><div>In this study, we conducted up to three cesarean sections (CS) on full-term pregnant mice, since a history of multiple CS is an independent risk factor for PAS. We evaluated pregnancy outcomes, placental development, morphology, trophoblast invasion, and angiogenesis at the maternal-fetal interface to assess the impact of repeated CS.</div></div><div><h3>Results</h3><div>Following repeated CS, the model mice displayed adverse pregnancy outcomes, including placental dysplasia, incomplete remodeling of spiral arteries, deep trophoblast invasion at the maternal-fetal interface, and reduced placental perfusion. Additionally, the mice exhibited abnormal fetal development, imbalances in angiogenic and anti-angiogenic both within the placenta and in peripheral blood.</div></div><div><h3>Conclusion</h3><div>The pathological phenotypes of placenta and adverse pregnancy outcomes observed in mice with a history of three CSs closely resemble the clinical features of PAS. This model offers a valuable tool for studying the pathogenesis of PAS and could serve as a foundation for the development of early prevention strategies.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"158 ","pages":"Pages 338-346"},"PeriodicalIF":3.0,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700646","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":"Understanding the impact of placental oxidative and nitrative stress in pregnancies complicated by fetal growth restriction","authors":"India A. Brooker ,&nbsp;Joshua J. Fisher ,&nbsp;Jessie M. Sutherland ,&nbsp;Kirsty G. Pringle","doi":"10.1016/j.placenta.2024.11.005","DOIUrl":"10.1016/j.placenta.2024.11.005","url":null,"abstract":"<div><div>Fetal growth restriction (FGR) impacts approximately 10 % of all pregnancies worldwide and is associated with major adverse effects on fetal health in both the short- and long-term [1]. FGR most commonly arises as a result of impaired placentation, occurring in up to 60 % of cases in developed countries [2]. This narrative review outlines the impact of defective placentation on the placenta, focusing on redox imbalance, how this leads to placental oxidative and nitrative stress, and the implications of these stressors on placental nutrient transfer, premature replicative senescence, and trophoblast cell death. Furthermore, this review highlights the pivotal role of antioxidants in protecting against oxidative and nitrative damage by reducing the burden of reactive species. We explore how targeting antioxidants in pregnancy provides a promising strategy for preventing or treating FGR, to ultimately reduce the devastating burden of FGR on infant health.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"158 ","pages":"Pages 318-328"},"PeriodicalIF":3.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693055","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":"Placental histopathology in early-onset fetal growth restriction with use of sildenafil, a secondary analysis of the Dutch STRIDER study","authors":"Marjon E. Feenstra ,&nbsp;Mirthe H. Schoots ,&nbsp;Romy Bezemer ,&nbsp;Lotte-Elisabeth van der Meeren ,&nbsp;Peter GJ. Nikkels ,&nbsp;Harry van Goor ,&nbsp;Jan-Luuk Hillebrands ,&nbsp;Jelmer R. Prins ,&nbsp;Wessel Ganzevoort ,&nbsp;Sanne J. Gordijn","doi":"10.1016/j.placenta.2024.10.024","DOIUrl":"10.1016/j.placenta.2024.10.024","url":null,"abstract":"<div><h3>Objectives</h3><div>Placental pathology lesions are common in early-onset fetal growth restriction (eoFGR). Therapeutic interventions to improve eoFGR outcomes are needed. In the international STRIDER trials (Sildenafil Therapy In Dismal prognosis Early-onset intrauterine growth Restriction) sildenafil didn't improve perinatal outcomes of eoFGR. We aimed to study the underlying placental pathology in the Dutch STRIDER trial and the effects of sildenafil on placental histopathology by describing the associations with sildenafil treatment, placental-dysfunction serum biomarkers and markers of oxidative stress.</div></div><div><h3>Methods</h3><div>The Dutch STRIDER trial was a randomized controlled trial of sildenafil versus placebo in 216 singleton pregnancies complicated by eoFGR, included between 20+0- and 29+6-weeks’ gestation. In 158 cases, placental histology was available. Lesions were classified independently by three perinatal pathologists blinded for clinical data, according to the international criteria of the Amsterdam Placental Workshop Group Consensus Statement. Blood samples taken at inclusion were analyzed for free thiols (FT), placental growth factor (PlGF) and soluble FMS-like tyrosine kinase-1 (sFlt-1, n = 85).</div></div><div><h3>Results</h3><div>The ‘big four’ placental lesions (maternal and fetal vascular malperfusion, and chronic or acute inflammatory lesions) were equally distributed in both groups. However, massive perivillous fibrin deposition (MPFD) and chronic histiocytic intervillositis (CHIV) were less common in the sildenafil-treated group compared to the placebo-treated group (p = 0.026 and p = 0.043). FT, PlGF and sFlt-1 at inclusion were not discriminative for placental lesions.</div></div><div><h3>Conclusions</h3><div>Sildenafil had no effect on common placental lesions. The lower incidence of MPFD and CHIV after sildenafil exposure merits more research on the interaction between sildenafil and the immune system.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"159 ","pages":"Pages 39-46"},"PeriodicalIF":3.0,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142745254","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":"Development and validation of the placenta-QUS model for the detection of placenta-mediated diseases using quantitative ultrasound measurements: An Ex Vivo proof-of-concept study","authors":"Farah Deeba ,&nbsp;Ricky Hu ,&nbsp;Victoria Lessoway ,&nbsp;Jefferson Terry ,&nbsp;Denise Pugash ,&nbsp;Chantal Mayer ,&nbsp;Jennifer Hutcheon ,&nbsp;Robert Rohling","doi":"10.1016/j.placenta.2024.11.004","DOIUrl":"10.1016/j.placenta.2024.11.004","url":null,"abstract":"<div><h3>Introduction</h3><div>Placenta-mediated diseases are associated with structural changes in the placenta. Quantitative Ultrasound (QUS) imaging measures the acoustic properties of the tissue, which are correlated to the underlying tissue structure. We aimed to develop and validate a diagnostic prediction model using QUS measurements for pre-eclampsia (PE) and small-for-gestational-age (SGA) fetuses/neonates.</div></div><div><h3>Methods</h3><div>For this prospective case-control study, placentas were collected from a group of women who delivered via cesarean section at BC Women's Hospital, Vancouver, Canada. Ultrasound data were collected and processed to compute three QUS parameters, namely, attenuation coefficient estimate (ACE), integrated backscatter coefficient (IBC), and effective scatterer diameter (ESD) from the placentas. We developed a logistic regression model using QUS parameters as predictors. The primary outcome was the occurrence of SGA and PE.</div></div><div><h3>Results</h3><div>The dataset consisted of 47 placentas, of which 25 placentas were complicated by SGA/PE. The final placenta-QUS model included quadratic and interaction terms of ACE, IBC, and ESD parameters. The placenta-QUS model was well-calibrated, with a calibration slope of 0.99 (0.57–1.05) and a calibration intercept of 0.003 (−0.02 − 0.22). The model predicted the SGA/PE complicated pregnancies with an apparent Area Under the Receive Operating Characteristic Curve (AUROC) of 0.89 (95 % CI: 0.78–0.98). The optimism-adjusted AUROC was 0.88 (95 % CI: 0.78–0.98).</div></div><div><h3>Discussion</h3><div>A model for SGA and PE has been developed using QUS measures from the placenta <em>ex vivo</em>. The model showed promising performance in detecting SGA/PE. Future studies will be performed to assess the model performance using QUS measures <em>in utero</em>.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"158 ","pages":"Pages 293-300"},"PeriodicalIF":3.0,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644399","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":"Aspartame intake during pregnancy induces placental dysfunction through impaired mitochondrial function and biogenesis modulation","authors":"Yang-Ching Chen ,&nbsp;Yen-Chia Yeh ,&nbsp;Yu-Fang Lin ,&nbsp;Shih-Yuan Hsu ,&nbsp;Jacus S. Nacis ,&nbsp;Jhih-Wei Hsu ,&nbsp;Rong-Hong Hsieh","doi":"10.1016/j.placenta.2024.11.003","DOIUrl":"10.1016/j.placenta.2024.11.003","url":null,"abstract":"<div><h3>Introduction</h3><div>Aspartame is a nonnutritive sweetener (NSS), which is widely used in foods and beverages worldwide. The safety of aspartame, a commonly used artificial sweetener, has been debated. Here, we investigated the potential effects and underlying mechanisms of aspartame consumption during pregnancy on placental dysfunction and birth outcomes.</div></div><div><h3>Methods</h3><div>Female Sprague Dawley rats were exposed to a low (30 mg/kg) or high (60 mg/kg) dose of aspartame before and during pregnancy; moreover, we assessed placental histopathological structure, oxidative stress markers, and mitochondrial function. In addition, we explored how aspartame affects birth weight in a human maternal–infant cohort.</div></div><div><h3>Results</h3><div>In animal study revealed that aspartame treatment of female rats for 14 weeks (12 week before pregnancy and 18 days of gestation) causes a significant reduction in the number and weight of fetuses, as well as damage to placental structure. These effects are linked to increased oxidative stress in the placenta, possibly damaging placental trophoblasts, impairing mitochondrial function, and initiating a compensatory mitochondrial biosynthesis mechanism. In the human pregnant cohort revealed that aspartame reduces birth weight considerably.</div></div><div><h3>Discussion</h3><div>These findings suggested the potential risks associated with aspartame consumption during pregnancy. Therefore, the safety of aspartame, particularly in pregnant individuals, should be reconsidered; specifically, tailored, acceptable daily intake guidelines should be developed for aspartame in different populations.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"158 ","pages":"Pages 285-292"},"PeriodicalIF":3.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639571","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":"Trophoblast proliferation is higher in female than in male preeclamptic placentas","authors":"N. Barapatre ,&nbsp;L. Hansen ,&nbsp;C. Kampfer ,&nbsp;T. Rübelmann ,&nbsp;C. Schmitz ,&nbsp;F. von Koch ,&nbsp;H.G. Frank","doi":"10.1016/j.placenta.2024.10.016","DOIUrl":"10.1016/j.placenta.2024.10.016","url":null,"abstract":"<div><h3>Introduction</h3><div>Preeclampsia (PE) is a pregnancy-specific hypertensive disorder with inflammatory complications. There are no known placental histopathological features, which are unique to PE. It is often pooled with the fetal growth restriction (FGR) under a single umbrella pathophysiology, the maternal vascular malperfusion (MVM). The aim of this study is to assess the villous trophoblast and the villous tree quantitatively in PE placentas and to identify morpholgical correlates unique to PE.</div></div><div><h3>Methods</h3><div>20 PE placentas (10 female and 10 male) and 20 Control placentas (10 female and 10 male) were included in the study. The villous trophoblast and the villous tree were assessed quantitatively by Stereology and 3D Microscopy. For Stereology measurements, the villous tree was classified in contractile and non-contractile parts based on immunohistochemical detection of perivascular myofibroblasts.</div></div><div><h3>Results</h3><div>The density of proliferative trophoblast nuclei is increased, whereas the density of non-proliferative trophoblast nuclei is decreased in female PE placentas. The male PE placentas do not show this effect. Though no significant difference in the diffusion distance was observed, the non-contractile villi and the fetal vessels inside show a significantly reduced volume in PE placentas. The branching index of the villous tree is lower in PE placentas in general. However, in female PE placentas the deviation is accentuated.</div></div><div><h3>Conclusion</h3><div>In PE, the villous trophoblast shows a sexually dimorphic alteration in the density of proliferative and non-proliferative nuclei, which is inherently different from FGR.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"158 ","pages":"Pages 310-317"},"PeriodicalIF":3.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644403","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}