Placenta最新文献

{"title":"Association between serum corin in the second trimester and hypertensive disorders of pregnancy: a mendelian randomization study","authors":"Xueyang Zhang ,&nbsp;Qing Yu ,&nbsp;Junjiang Liu ,&nbsp;Pei Feng ,&nbsp;Wenxiu Fan ,&nbsp;Yibing Jin ,&nbsp;Xiangdong Yang ,&nbsp;Hongmei Li ,&nbsp;Lei Wu ,&nbsp;Hao Peng","doi":"10.1016/j.placenta.2025.07.091","DOIUrl":"10.1016/j.placenta.2025.07.091","url":null,"abstract":"<div><h3>Background</h3><div>Serum corin has been associated with hypertensive disorders of pregnancy (HDP) in clinical studies but lacks causal evidence. This study aimed to systemically examine the associations of serum corin and its coding gene polymorphisms with HDP, as well as the underlying causality among Chinese pregnant women.</div></div><div><h3>Methods</h3><div>A nested case-control study comprising 403 cases of HDP and 402 age- and parity-matched healthy controls was designed. Serum corin and its coding gene genotype (19 SNPs) were assayed before 20 gestational weeks. Their associations with HDP were systemically examined using gene-based and Mendelian Randomization (MR) approaches.</div></div><div><h3>Results</h3><div>Serum corin was negatively associated with HDP (OR = 0.92, 95 %CI: 0.88–0.96, <em>P</em> = 0.025) even after adjusting for conventional risk factors. Most SNPs genotyped were associated with serum corin but none of them were associated with HDP, either individually or jointly (all <em>P</em> &gt; 0.05). The MR analysis based on our own or summary data failed to observe a significant causal relationship between corin and HDP (<em>P</em> &gt; 0.05).</div></div><div><h3>Conclusion</h3><div>Deficient serum corin in early pregnancy indicates, but may not causally, an increased risk of HDP in Chinese women. The clinical translation of corin into HDP management needs further study.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 107-113"},"PeriodicalIF":2.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757193","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":"Establishment of human trophoblast stem cells from term smooth chorion","authors":"Takako Hoshiyama ,&nbsp;Masanaga Muto ,&nbsp;Shoma Matsumoto ,&nbsp;Eiichi Okamura ,&nbsp;Bat-Erdene Jargalsaikhan ,&nbsp;Takashi Murakami ,&nbsp;Shunichiro Tsuji ,&nbsp;Masatsugu Ema","doi":"10.1016/j.placenta.2025.07.090","DOIUrl":"10.1016/j.placenta.2025.07.090","url":null,"abstract":"<div><h3>Introduction</h3><div>Human trophoblast stem (TS) cells derived from first-trimester placental villi (TS^CT) and blastocyst (TS^blast) are valuable for studying placental development and pathobiology. However, most placenta-mediated pregnancy complications are diagnosed in the third-trimester, and there are limited reports on TS cells from the third-trimester placental tissues. In this study, we report the successful derivation of TS cells from the term smooth chorion.</div></div><div><h3>Methods</h3><div>Smooth chorion isolation was carried out from term placenta, followed by the preparation of single cells through enzymatic dissociation. ITGA6-positive cells were isolated from smooth chorion and cultured in TS medium. The chorion-derived TS (Ch-TS) cells were characterized through flow cytometry, immunocytochemical analysis, DNA methylation analyses via bisulfite sequencing, miRNA analysis using quantitative PCR, and RNA sequencing. To assess their differentiation potential, Ch-TS cells were induced to differentiate into extravillous trophoblast (EVT) cells and syncytiotrophoblast (ST) cells.</div></div><div><h3>Results</h3><div>Human TS cells were successfully derived from the term smooth chorion. Immunohistochemistry confirmed trophoblast marker expression in Ch-TS cells. Bisulfite sequencing revealed that the <em>ELF5</em> promoter region was hypomethylated in Ch-TS cells, consistent with trophoblastic DNA methylation status. Ch-TS cells expressed miRNAs from the chromosome 19 miRNA cluster (C19MC). Flow cytometryanalysis revealed that the expression patterns of HLA class I molecules were comparable between Ch-TS and TS^CT/blast. Ch-TS cells successfully differentiated into EVT and ST cells. RNA sequencing showed transcriptomic similarities between Ch-TS cells and TS^CT^/blast cells.</div></div><div><h3>Discussion</h3><div>Ch-TS cells may serve as a valuable <em>in vitro</em> model for studying trophoblast biology and placenta-mediated pregnancy complications, similar to TS^CT^/blast cells.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 114-122"},"PeriodicalIF":2.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144763613","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":"Reduced level of BMI1 inhibits trophoblast proliferation and migration via the epigenetic enhancement of CSTA and TGFB2 in spontaneous abortion","authors":"Huimin Li ,&nbsp;Gaigai Wang ,&nbsp;Qingxia Meng ,&nbsp;Rui Zhu ,&nbsp;Minjuan Liu ,&nbsp;Xiangyun Zhang ,&nbsp;Jiaxiong Wang ,&nbsp;Hong Li","doi":"10.1016/j.placenta.2025.07.087","DOIUrl":"10.1016/j.placenta.2025.07.087","url":null,"abstract":"<div><h3>Introduction</h3><div>Spontaneous abortion is the loss of a pregnancy before the 28th week of gestation in China. The precise mechanisms leading to spontaneous abortion remain largely unclear.</div></div><div><h3>Methods</h3><div>The expression of BMI1 in normal pregnancy and SA villous tissues was detected by qRT-PCR and immunofluorescence staining. Cell proliferation, migration, and apoptosis were assessed to explore the role of BMI1 in HTR-8/SVneo cells. Integrated RNA-seq and ChIP-seq analysis identified direct targets involved in the effects of BMI1 on trophoblasts.</div></div><div><h3>Results</h3><div>Individuals with SA exhibited reduced levels of BMI1 in villous tissues. The knockdown of BMI1 inhibited the proliferation, clonogenicity, and migration of trophoblast cells but enhanced apoptosis. BMI1 overexpression induced the opposite effects. Moreover, we observed enhanced proliferation, migration, and colony formation in cells that had been treated with PTC-209 and a diverse range of NAC concentrations when compared to cells treated with PTC-209 alone. Despite the reduction of ROS, complete recovery of the cellular phenotype could not be achieved. CSTA and TGFB2 were identified as direct target molecules of BMI1. Specifically, overexpression of CSTA significantly reduced the levels of phosphorylated AKT, while overexpression of TGFB2 induced a notable increase in phosphorylated SMAD2/3 proteins. Finally, cell rescue assays demonstrated that the suppression of CSTA and TGFB2 counteracted the effects of BMI1 deficiency on trophoblasts.</div></div><div><h3>Discussion</h3><div>The regulation of trophoblast function by BMI1, including the production of ROS in the cytoplasm and the epigenetic modifications of CSTA and TGFB2 in nuclei, could facilitate the identification of mechanisms underlying SA.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 82-93"},"PeriodicalIF":2.5,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144724274","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":"Ferroptosis as a mechanism of placenta dysfunction in inflammation-driven preeclampsia","authors":"Yusmaris Cariaco ,&nbsp;Megan Beck ,&nbsp;Fahmida Jahan ,&nbsp;Jade Gamelin Kao ,&nbsp;Abolfazl Nik-Akhtar ,&nbsp;Keir Menzies ,&nbsp;Shannon Bainbridge","doi":"10.1016/j.placenta.2025.07.085","DOIUrl":"10.1016/j.placenta.2025.07.085","url":null,"abstract":"<div><h3>Background</h3><div>Preeclampsia (PE) is a hypertensive pregnancy syndrome with significant clinical and pathological diversity, linked to distinct etiological subclasses. One etiological subclass of PE, characterized by increased inflammation at the maternal-fetal interface (I-PE), is strongly associated with preterm birth and fetal growth restriction, though its specific pathophysiology remains poorly understood. Inflammatory signals can induce iron overload, leading to ferroptosis—a programmed cell death process. Dysregulation of systemic and placental iron metabolism has been described in PE when considered as a single clinical entity, but previous studies have not accounted for distinct underlying etiologies. This study investigates the role of ferroptosis signaling in placental dysfunction across different PE subclasses.</div></div><div><h3>Methods</h3><div>Histological analysis assessed placental iron accumulation and ferritin protein expression. Placental gene expression was evaluated for ferroptosis-related genes (FRGs) using gene set enrichment analysis (GSEA) on placenta samples from healthy controls and three previously described PE subclasses. Digital cytometry estimated cell type-specific expression of FRGs across these subclasses.</div></div><div><h3>Results</h3><div>Significant placenta iron accumulation and reduced ferritin expression were found exclusively in I-PE subclass. GSEA showed enrichment of FRGs across various functional categories, including regulators, markers, suppressors, and unclassified FRGs in the placentas from I-PE. Digital cytometry indicated disrupted FRG expression in trophoblasts and mesodermal stromal cells in these placentas, consistent with histologically observed iron accumulation.</div></div><div><h3>Conclusion</h3><div>Placental iron accumulation and disrupted ferroptosis signaling in I-PE subclass suggests a novel mechanism of placental dysfunction unique to this subclass. Further research is needed to explore how regulating ferroptosis could aid in managing I-PE.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 94-106"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144724275","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":"Monocyte chemoattractant Protein-1 (MCP-1) decreases mineralization of the villous stroma in the macaque placenta","authors":"Logan T. Keding ,&nbsp;Jessica Vazquez ,&nbsp;Ruo-Yu Liu ,&nbsp;Emily Bove ,&nbsp;Jessica Dorobek ,&nbsp;Heather A. Simmons ,&nbsp;Kathleen M. Antony ,&nbsp;Jenna L. Racine ,&nbsp;Dinesh M. Shah ,&nbsp;Oliver Wieben ,&nbsp;Thaddeus G. Golos ,&nbsp;Aleksandar K. Stanic","doi":"10.1016/j.placenta.2025.07.083","DOIUrl":"10.1016/j.placenta.2025.07.083","url":null,"abstract":"<div><h3>Introduction</h3><div>Placental insufficiency occurs when a fetus does not receive adequate oxygen and/or nutrients, leading to adverse pregnancy outcomes (APOs). Increased leukocyte density has been observed in placental inflammatory lesions, resulting in placental insufficiency and APOs. MCP-1 is a chemokine associated with inflammatory disease, that actively attracts leukocyte populations. We investigated the effects of a supraphysiological MCP-1 injection into the maternal-fetal interface (MFI), using the macaque pregnancy model.</div></div><div><h3>Methods</h3><div>A placental injection of MCP-1 or saline was administered to macaques between gestational day (GD) 100–105, along the MFI. Acute effects (n = 2) and full-term effects (n = 8) were studied. Full-term pregnancies had maternal placental blood perfusion measured via dynamic contrast enhanced MRI, before and after injection. Fetoplacental tissues were collected near term (GD 155). Placental histopathology was investigated, along with decidual immune populations, MRI-defined maternal blood metrics, and fetal biometrics.</div></div><div><h3>Results</h3><div>Acutely, increased leukocyte clustering and decreased mineralization were observed within the villous stroma of MCP-1-treated cotyledons. Decreased villous mineralization with MCP-1 injection was also noted in full-term pregnancies, along with a proportional increase in decidual dendritic cells. MRI placental analysis revealed a trend of increased maternal blood flow and reduced fill time after MCP-1 injection, alongside healthy fetal biometrics.</div></div><div><h3>Discussion</h3><div>Although MCP-1 is typically associated with inflammation and tissue pathology, our study demonstrates that supraphysiological MCP-1 levels led to increased leukocyte clustering and reduced mineralization in the villous stroma, without impairing maternal blood perfusion or fetal growth. These findings suggest a beneficial role for MCP-1 in the context of placental function.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 72-81"},"PeriodicalIF":2.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722779","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":"NOTCH, WNT, and TGFβ: Key pathways in extravillous trophoblast formation and differentiation.","authors":"Gudrun Meinhardt, Sandra Haider","doi":"10.1016/j.placenta.2025.07.082","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.07.082","url":null,"abstract":"<p><p>During gestation, the human placenta ensures nutrition, gas exchange, and protection against pathogens for the growing fetus. As key component in placentation, extravillous trophoblasts (EVTs) arise from trophoblast (TB) progenitors through extensive proliferation at placental tip structures. A stepwise and tightly orchestrated differentiation process enables post-proliferative EVTs to invade maternal uterine layers, remodel the uterine vasculature, and modulate the maternal immune system to sustain pregnancy. Various signaling pathways are crucial in TB biology, including the MAPK, WNT, NOTCH, HIPPO, EGFR, and TGFβ cascades, which have been the subject of numerous comprehensive reviews. Recently developed TB model systems such as TB stem cells and TB organoids have significantly advanced placental research by enabling precise manipulation of signaling pathways and control over TB lineage determination and differentiation. Building on these advancements, this review specifically examines the activity and role of NOTCH, WNT, and TGFβ signaling in the sequential steps of EVT differentiation, integrating key insights gained from TB stem cell- and TB organoid-based studies.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718325","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":"Downregulation of ANXA2 suppresses trophoblast cell invasion and migration through β-catenin pathway in preeclampsia","authors":"Zhengrong Mei ,&nbsp;Mingjie Gong ,&nbsp;Jianqi Lai,&nbsp;Pei Liu,&nbsp;Ying Wang,&nbsp;Peili Du,&nbsp;Fang He","doi":"10.1016/j.placenta.2025.07.076","DOIUrl":"10.1016/j.placenta.2025.07.076","url":null,"abstract":"<div><div>Preeclampsia (PE) is a multisystem progressive disease unique to pregnancy, the pathogenesis of PE is thought to be linked to inadequate trophoblast invasion. Annexin a2 (ANXA2) has been found to be closely related to tumor metastasis and it may be involved in trophoblast invasion. Evidence from translational oncology research indicates that ANXA2 overexpression drives metastatic progression in malignancies via canonical Wnt/β-catenin pathway activation, particularly through stabilization of cytoplasmic β-catenin and subsequent nuclear translocation. The Wnt/β-catenin signaling pathway is an important pathway in placental implantation and embryonic development. This study aims to elucidate the role of ANXA2 in the progression of PE. ANXA2 expression in PE placentas was analyzed using Western blotting and immunohistochemistry. The cell proliferation, invasion, and migration were assessed using MTT assay, transwell, and wound healing assays. Our findings indicate a significant reduction in ANXA2 expression in the placentas of PE patients compared to controls. ANXA2 knockdown in HTR-8/SVneo cells resulted in decreased cell proliferation, invasion, and migration. Conversely, overexpression of ANXA2 enhanced these cellular functions. Furthermore, knockdown of ANXA2 led to suppression of the β-catenin signaling pathway through the modulation of GSK-3β expression. The downregulation of ANXA2 contributes significantly to the pathogenesis of PE by impairing trophoblast invasion and migration via inhibition of the β-catenin signaling pathway. These findings highlight the critical role of ANXA2 in the development of PE and suggest that targeting ANXA2-related pathways may offer novel therapeutic avenues for the management of this disorder.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 60-71"},"PeriodicalIF":3.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144704193","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":"Effects of hyperhomocysteinemia on placental morphology and function","authors":"Yuan Zhang ,&nbsp;Ruiping Lu ,&nbsp;Yulan Ma ,&nbsp;Jie Ma ,&nbsp;Linlin Song ,&nbsp;Fanqing Zhou ,&nbsp;Jingwen Guo ,&nbsp;Rong Hu","doi":"10.1016/j.placenta.2025.07.074","DOIUrl":"10.1016/j.placenta.2025.07.074","url":null,"abstract":"<div><h3>Objective</h3><div>Hyperhomocysteinemia (HHcy), characterized by elevated homocysteine levels, is associated with adverse pregnancy outcomes, though its mechanistic link to placental dysfunction remains unclear. This study aimed to explore how HHcy disrupts placental development to identify conserved molecular mechanisms related to adverse pregnancy outcomes.</div></div><div><h3>Methods</h3><div>We develop murine HHcy model using a high-methionine diet and observe placental and fetal developmental outcome at key pregnancy times (E7.5, E10.5, E13.5). Structural and functional anomalies were detected histopathologically and molecularly to examine potential placental pathology. Expression profiles in placental tissues were determined by transcriptome profiling to describe dysregulated pathways. Expression and activity of lysosomal-autophagy were examined by qRT-PCR, western blotting, and transmission electron microscopy. Clinical validation was performed using placental samples from spontaneous abortion (SA) patients with HHcy and without HHcy and matched controls.</div></div><div><h3>Results</h3><div>HHcy-exposed mice exhibited significant reductions in embryo implantation rates and fetal viability, accompanied by impaired placental growth and structural disorganization. Histological analysis revealed atrophy of the ectoplacental cone, dilation of intervillous spaces, and diminished labyrinthine/junctional zones. Transcriptomic data highlighted enrichment of lysosomal and inflammatory pathways, corroborated by molecular evidence of lysosomal overload, suppressed autophagy-related gene expression and dysregulated autophagic flux. Placental samples from SA patients with HHcy mirrored these molecular alterations.</div></div><div><h3>Conclusion</h3><div>Our findings suggest that HHcy disrupts placental homeostasis, impairs lysosomal function, and triggers maladaptive autophagy, leading to adverse pregnancy outcomes. The conserved pathways suggest targeting the lysosomal - autophagic axis might treat HHcy - related pregnancy problems.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 21-29"},"PeriodicalIF":3.0,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144680266","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":"Gross patterns of umbilical cord coiling in pregnancies with and without gestational diabetes mellitus","authors":"Napaporn Puripat ,&nbsp;Chutima Chavanisakun ,&nbsp;Petcharat Jenkumwong ,&nbsp;Siriwan Tangjitgamol ,&nbsp;Chadakarn Phaloprakarn","doi":"10.1016/j.placenta.2025.07.080","DOIUrl":"10.1016/j.placenta.2025.07.080","url":null,"abstract":"<div><h3>Introduction</h3><div>Gestational diabetes mellitus (GDM) may influence the umbilical cord coiling index, but its effect on gross coiling patterns remains unclear. This study compared umbilical cord coiling patterns in pregnancies with GDM to those without and explored associations with placental pathology and adverse perinatal outcomes. The accuracy of antenatal ultrasound in detecting coil indentations and twist direction (sinistral or dextral) was also assessed.</div></div><div><h3>Methods</h3><div>In this prospective study, antenatal ultrasound and postpartum pathological examination were used to assess cord morphology in 200 women with GDM and 100 women without GDM. Ultrasound findings of coil indentations and twist direction were compared to postpartum diagnoses. Placental pathology, including fetal vascular malperfusion, and composite adverse outcomes—such as fetal heart rate decelerations, small-for-gestational-age neonates, low Apgar scores, and neonatal intensive care unit admissions—were analyzed.</div></div><div><h3>Results</h3><div>Coiling patterns and twist direction were similar between groups and showed no association with fetal vascular malperfusion. However, dextral (right-twisting) umbilical cords were significantly associated with a higher risk of adverse outcomes, even after adjusting for GDM status, gestational age at delivery, coiling index, and gross coiling pattern (adjusted odds ratio = 2.67 [95 % confidence interval 1.34, 5.32]). Antenatal ultrasound accurately detected twist direction in 100 % of cases.</div></div><div><h3>Conclusions</h3><div>Although umbilical cord morphology does not significantly differ between pregnancies with and without GDM, dextral coiling may indicate an increased risk of adverse perinatal outcomes. Given the high accuracy of ultrasound in detecting twist direction, incorporating this assessment into routine prenatal care may help improve monitoring and outcomes.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 14-20"},"PeriodicalIF":3.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144680265","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":"Investigating the abnormalities and potential therapeutic targets in umbilical cord mesenchymal stem cells from preeclampsia","authors":"Fei He ,&nbsp;We Cai ,&nbsp;Shaoru Cai ,&nbsp;Chupeng Ou ,&nbsp;Shuhe Lu ,&nbsp;Ziqing Huang ,&nbsp;Shao Li ,&nbsp;Shilei Pan","doi":"10.1016/j.placenta.2025.07.077","DOIUrl":"10.1016/j.placenta.2025.07.077","url":null,"abstract":"<div><h3>Background</h3><div>Damaged cells are influenced by their microenvironment, which may lead to abnormalities. In preeclampsia (PE), several abnormal changes can occur that affect the umbilical cord and, consequently, umbilical cord mesenchymal stem cells (UCMSCs). Understanding these mechanisms can optimize therapeutic strategies for UCMSCs, thereby in addressing a range of complex disease microenvironments.</div></div><div><h3>Methods</h3><div>Flow cytometry analysis, alizarin red staining and oil red O staining were utilized to detect the characteristic surface markers and assess the differentiation potential of UCMSCs. The CCK8 and EdU assays were used to assess cell proliferation. RNA sequencing was performed on UCMSCs from both donor groups. A senolytic combination therapy was applied to target senescent cells, with JC-1 fluorescence staining assay, SA-β-gal staining and gene expression to identify cellular senescence. Immunofluorescence analysis was conducted to examine proliferation and cytoskeletal changes.</div></div><div><h3>Results</h3><div>UCMSCs from both donor groups did exhibit significant differences in surface markers and differentiation capacity. UCMSCs-PE demonstrated reduced cell proliferation. Transcriptome analysis revealed notable alterations, particularly in senescence and cytoskeletal changes, which were validated by increased SA-β-gal activity, impaired mitochondrial function, and cytoskeletal staining. The senescence phenotype and cytoskeletal integrity in the UCMSCs-PE group were notably improved by the combination of dasatinib and quercetin.</div></div><div><h3>Conclusions</h3><div>Our study suggests that senescence and cytoskeletal abnormalities may represent notable changes in UCMSCs-PE. Cellular senescence may play a critical role in the physiology of PE, highlighting the potential of targeting senescence mechanisms as a novel approach.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"169 ","pages":"Pages 49-59"},"PeriodicalIF":3.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144704192","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}