Placenta最新文献

{"title":"Increased protein O-GlcNAcYLATION in human placentas from hypertensive pregnancies.","authors":"Marta de Lima Castro, Rinaldo Rodrigues Dos Passos, Thiago Lopes Rocha, Waldemar Naves do Amaral, Fernanda Regina Giachini","doi":"10.1016/j.placenta.2025.05.024","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.024","url":null,"abstract":"<p><strong>Introduction: </strong>Key proteins involved in placentation are susceptible to O-linked β-N-acetylglucosamine modification (O-GlcNAcylation). Anomalies in protein O-GlcNAcylation have been associated with pathological conditions, including hypertension, and it is known that arterial hypertension negatively impacts placental function. However, the precise impact of protein O-GlcNAcylation on placental function and fetal growth remains unclear in humans. Therefore, the current study aimed to investigate O-GlcNAcylation expression, and its catalytic enzyme O-GlcNAc transferase (OGT), in the placenta of pregnant women suffering from high blood pressure disorders.</p><p><strong>Methods: </strong>Full-term placental samples were collected and divided into groups of normotensives (n = 11) or hypertensives women (n = 11). Western blotting and immunohistochemistry assessed O-GlcNAc and OGT expressions, and morphological characterization was conducted in all samples.</p><p><strong>Results: </strong>In the hypertensive group, the maternal age (p = 0.041) was higher, whereas the gestational age (p = 0.004) and the newborn weight (p = 0.032) decreased, compared to the normotensive group. Morphometric analysis showed that the placentas from the hypertensive group displayed altered morphology, which was compatible with placentas from hypertensive mothers. Placental O-GlcNAc (p = 0.029) and OGT (p = 0.048) protein expression were higher in the hypertensive group. Augmented expression of O-GlcNAc was more predominant in the villi but also observed at the decidua.</p><p><strong>Discussion: </strong>The present study demonstrates augmented protein O-GlcNAcylation and OGT expression in the placenta of pregnant with hypertensive disorders of pregnancy. In the future, the use of banks of placental tissue may be a useful strategy to map and identify candidates for O-GlcNAc modulation, requiring further evaluation.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174692","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":"Placental growth factor enhances inflammatory toll-like receptor responses in syncytiotrophoblasts","authors":"Laura F. Newell ,&nbsp;Shernan G. Holtan ,&nbsp;Leena Kadam ,&nbsp;Grover C. Bagby ,&nbsp;Leslie Myatt","doi":"10.1016/j.placenta.2025.05.023","DOIUrl":"10.1016/j.placenta.2025.05.023","url":null,"abstract":"<div><h3>Introduction</h3><div>Pregnancy requires that the development of immune tolerance to avoid fetal rejection is balanced with functional immune surveillance mechanisms against infectious pathogens. Trophoblast cells play a unique role in influencing the state of maternal and fetal immune activation. Placental growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, is a placental-derived factor with maximal expression during early third trimester, when women are at particular risk of morbidity from viral infections. Having previously demonstrated that PlGF enhanced toll-like receptor (TLR)-mediated inflammatory cytokine expression in peripheral blood mononuclear phagocytes, we hypothesized that PlGF might also contribute to hyper-inflammatory TLR responses in the trophoblast.</div></div><div><h3>Methods</h3><div>Primary human syncytiotrophoblast cells were cultured in the presence of VEGF receptor-1 (VEGFR1) ligands (including the PlGF isoforms), with and without TLR-agonists.</div></div><div><h3>Results</h3><div>PlGF significantly increased TLR-mediated inflammatory cytokine production by syncytiotrophoblast cells in a time- and dose-dependent manner, and enhanced the magnitude of cytokine gene transcription. This PlGF/TLR effect was specific to PlGF-1, and PlGF-1 influenced the majority of but not all TLR-agonists.</div></div><div><h3>Discussion</h3><div>We determined that PlGF influences TLR-pathway activation in syncytiotrophoblast cells, in a similar manner to its effect in mononuclear phagocytes. These results suggest that PlGF contributes to an exaggerated hyper-inflammatory state in diverse cells of the innate immune system and in syncytiotrophoblast cells, in response to infectious stimuli. PlGF may play a key role in the increased maternal and fetal susceptibility to infection-mediated inflammatory complications during pregnancy.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"168 ","pages":"Pages 9-18"},"PeriodicalIF":3.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144178016","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":"Inflammation-induced TET3/mir-3942 axis impedes the proliferation and invasion ability of trophoblast cells through destabilization of SERPINE1 in preeclampsia","authors":"Xiaokang Deng ,&nbsp;Qing Zuo ,&nbsp;Yi Liu ,&nbsp;Meilikang Li ,&nbsp;Liuxin Wu ,&nbsp;Jingling Jiang ,&nbsp;Juveria Rahman ,&nbsp;Matthew Sagnelli ,&nbsp;Tingting Zhang ,&nbsp;Lizhou Sun ,&nbsp;Yetao Xu","doi":"10.1016/j.placenta.2025.05.022","DOIUrl":"10.1016/j.placenta.2025.05.022","url":null,"abstract":"<div><h3>Introduction</h3><div>Abnormal expression of TET3 has been established to be associated with aberrant function of trophoblasts and lead to the progression of Preeclampsia (PE). Yet, the underlying mechanism of PE mediated by TET3 has not been elucidated.</div></div><div><h3>Methods</h3><div>Target factors downstream of TET3 were identified by RNA-seq. Functional assays were used to assess the effects of TET3/SERPINE1 on the proliferation and invasion capabilities of HTR-8 and JAR. ChIP-PCR and Targeted bisulfite sequencing were conducted to detect the demethylation in the SERPINE1 promoter after inhibition of TET3. Luciferase reporter assays were performed to elucidate the mechanism by which miR-3942 binds to TET3/SERPINE1 mRNA. TET3 knockout mice and uterine artery ligation mice to further verify the reliability of this conclusion.</div></div><div><h3>Results</h3><div>First, we identified genes mediated by TET3 in HTR-8 by RNA-seq. Then, we focus on SERPINE1 as the special downstream gene. The resulting data showed that SERPINE1 could reduce the proliferation and invasion. RNA-seq and mechanism analysis indicated that inhibition of <em>TET3</em> suppressed the activation of SERPINE1 by reducing the demethylation of related CpG sites in the SERPINE1 promoter, thereby transcriptionally inactivating SERPINE1 expression. Moreover, luciferase reporter assay indicates that <em>TET3</em> and SERPINE1 were direct targets of miR-3942. At last inflammatory cytokines may stimulate trophoblasts to enhance TET3 expression, promoting demethylation of SERPINE1 promoter and inducing SERPINE1 expression.</div></div><div><h3>Discussion</h3><div>This study uncovers a <em>TET3</em>-mediated regulatory mechanism which can be stimulate by inflammatory cytokines in PE progression and suggests that targeting the miR-3942-TET3-SERPINE1-axis may provide new predictive and therapeutic interventions for PE.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 193-203"},"PeriodicalIF":3.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144134247","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":"Reframing the paradigm-rethinking placental and fetal immunity.","authors":"Liza Konnikova","doi":"10.1016/j.placenta.2025.05.011","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.011","url":null,"abstract":"<p><p>Preterm birth (PTB), defined as delivery before 37 weeks of gestation, is a leading cause of infant mortality worldwide, with nearly 10 % of births in the U.S. being preterm. PTB leads to various complications, including respiratory, neurological, and immunological issues, along with long-term health problems. It also costs the U.S. healthcare system approximately $25 billion annually, impacting families with lost productivity and long-term care needs. Understanding fetal and placental immunity is critical in addressing PTB. The immune system plays a vital role in maternal tolerance to the fetus and fetal immune development. Research into immune cells and signaling within the placenta may help prevent complications leading to PTB. Additionally, the interaction between maternal and fetal immune systems could reveal therapeutic targets to reduce preterm labor. Although animal models, especially mice, have advanced our understanding of fetal immunity, their differences from humans limit their applicability. Human studies, particularly those examining cord blood, had shown that neonatal immune cells are naïve at birth. However closer examination of preterm infants' blood demonstrated that they exhibit memory T cells linked to preterm labor. Building on this discovery, data demonstrates that fetal memory T cells exist in numerous fetal organs including the placenta. As such, research indicates that the fetus actively shapes the immune environment within the placenta. Disruptions in this process may contribute to PTB. Future investigations into fetal trained immunity and how to improve fetal immune responses could enhance neonatal protection. Understanding immune development in utero could lead to interventions that optimize neonatal health and prevent infections.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144161697","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":"Endoplasmic reticulum stress induces trophoblast pyroptosis via regulating CYLD during labor initiation","authors":"Xiaolei Zhang ,&nbsp;Meitao Yang ,&nbsp;Dan Lv ,&nbsp;Yanling Zhang ,&nbsp;Yin Xie ,&nbsp;Mengzhou He ,&nbsp;Yao Fan ,&nbsp;Xufang Li ,&nbsp;Fatoumata Jallow ,&nbsp;Fanfan Li ,&nbsp;Dongrui Deng","doi":"10.1016/j.placenta.2025.05.020","DOIUrl":"10.1016/j.placenta.2025.05.020","url":null,"abstract":"<div><h3>Introduction</h3><div>Preterm birth (PTB) presents significant risks to neonatal health, highlighting a deeper understanding of the mechanisms underlying labor initiation. Maternal-fetal interface inflammation and heightened endoplasmic reticulum stress (ERS) are associated with the onset of PTB, while the molecular mechanism remains unclear. This study investigates ERS levels in placental tissues from term and preterm pregnancies and examines the role of ERS and cylindromatosis (CYLD) in trophoblast pyroptosis to reveal the mechanisms underlying PTB.</div></div><div><h3>Methods</h3><div>A total of 60 pregnant women were recruited and categorized into four groups: term labor (TL), term not in labor (TNL), preterm labor (PTL), and preterm not in labor (PTNL). Protein expressions of ERS and pyroptosis-related molecules, including CYLD, were assessed using Western blotting, immunohistochemistry, and immunofluorescence. IL-1β and IL-18 mRNA levels were quantified via real-time PCR. An in vitro inflammatory trophoblast model was established using LPS and ATP co-treatment. ERS modulation was achieved with Thapsigargin (TG) and Tauroursodeoxycholate (TUDCA).</div></div><div><h3>Results</h3><div>Elevated ERS and pyroptosis-related protein levels were observed in PTB-associated groups and the inflammatory trophoblast model. TG increased CYLD expression and induced cell pyroptosis, while TUDCA mitigated these effects. CYLD silencing reduced trophoblast pyroptosis, whereas overexpression negated TUDCA's inhibitory impact.</div></div><div><h3>Discussion</h3><div>Our findings indicate that ERS-mediated trophoblast pyroptosis via CYLD under inflammatory conditions sheds light on PTB mechanisms, providing a potential target for modulating labor onset.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 204-215"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131022","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":"Growth differentiation factor-8 promotes human extravillous trophoblast cell invasion by increasing ANGPTL4 expression","authors":"Shenghui Zhou ,&nbsp;Beibei Bi ,&nbsp;Ze Wu,&nbsp;Siwei Luo,&nbsp;Manman Guo,&nbsp;Jung-Chien Cheng,&nbsp;Lanlan Fang","doi":"10.1016/j.placenta.2025.05.021","DOIUrl":"10.1016/j.placenta.2025.05.021","url":null,"abstract":"<div><h3>Introduction</h3><div>Proper regulation of extravillous trophoblast (EVT) cell invasion is critical for normal placental development and function. Angiopoietin-like 4 (ANGPTL4), a multifunctional protein, has previously been implicated in promoting EVT cell invasion. Growth differentiation factor-8 (GDF-8), a member of the transforming growth factor-β (TGF-β) superfamily, also stimulates EVT cell invasion. However, it remains unclear whether GDF-8 regulates ANGPTL4 expression and how this regulation contributes to the invasive behavior of human EVT cells. This study aims to explore the role of ANGPTL4 in GDF-8-induced EVT cell invasion and to uncover the underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>The immortalized EVT cell line HTR-8/SVneo and primary human EVT cells were used as <em>in vitro</em> models. The effects of GDF-8 on ANGPTL4 expression and the underlying signaling mechanisms were investigated using RT-qPCR and Western blot analysis. Cell viability was assessed using the MTT assay, and cell invasiveness was examined using a Matrigel-coated transwell invasion assay.</div></div><div><h3>Results</h3><div>Our results demonstrated that GDF-8 increased ANGPTL4 expression. Mechanistically, we found that activin receptor-like kinases 4 and 5 (ALK4 and ALK5) were required for GDF-8-mediated upregulation of ANGPTL4. Additionally, both SMAD2 and SMAD3 were involved in this regulatory pathway. We further showed that GDF-8 treatment promoted cell invasion without affecting cell viability. The pro-invasive effect of GDF-8 was attenuated by ANGPTL4 knockdown, whereas ANGPTL4 overexpression alone enhanced cell invasiveness.</div></div><div><h3>Discussion</h3><div>This study reveals a novel role for GDF-8 in regulating ANGPTL4 expression and EVT cell invasion, offering new insights into placental development and potential implications for pregnancy-related disorders.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 227-235"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139112","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":"Correlation between first trimester placental growth factor levels and skin microvascular reactivity assessed by laser speckle contrast imaging - a cross-sectional study","authors":"Mor Huri ,&nbsp;Isabella Abati ,&nbsp;Chiara Bartolini ,&nbsp;Alessia Piacenza ,&nbsp;Lorenzo Tofani ,&nbsp;Arianna Vallario ,&nbsp;Mariarosaria Di Tommaso ,&nbsp;Viola Seravalli","doi":"10.1016/j.placenta.2025.05.019","DOIUrl":"10.1016/j.placenta.2025.05.019","url":null,"abstract":"<div><h3>Objectives</h3><div>To investigate the association between first-trimester placental growth factor (PlGF) levels and maternal skin microvascular reactivity, as assessed by laser speckle contrast imaging (LSCI) combined with post-occlusive reactive hyperemia. Additionally, to explore the correlations between maternal microvascular function and other first-trimester serum biochemical and biophysical markers.</div></div><div><h3>Methods</h3><div>Fifty-three patients carrying a singleton gestation were enrolled during their routine first trimester scan. Skin blood flux at the dorsal hand was recorded using LSCI before, during, and after a 3-min arterial occlusion. Microvascular reactivity parameters were calculated and compared with maternal serum biochemical markers (PlGF, pregnancy-associated plasma protein A [PAPP-A], and free beta-human chorionic gonadotropin [free β-hCG]), expressed as multiples of the median, and with maternal biophysical markers.</div></div><div><h3>Results</h3><div>PlGF levels showed a moderate positive correlation with base-to-peak flux (r = 0.51, 95 % confidence interval, CI, 0.27–0.69) and a weak but statistically significant positive correlation with peak flux (r = 0.31, 95 % CI 0.04–0.59).</div><div>PAPP-A levels above the median were associated with higher base-to peak flux compared to PAPP-A below the median (253.41 % versus 215.08 %, p = 0.02). A moderate positive correlation was also found between free β-hCG and peak flux (r = 0.4, 95 % CI 0.15–0.60). No correlations were found between the parameters of hyperemic response and maternal biophysical markers.</div></div><div><h3>Conclusions</h3><div>Maternal first-trimester skin microvascular reactivity indices correlate positively with serum placental biomarker levels, particularly PlGF. This suggests that maternal peripheral microvascular function, assessed by LSCI, may reflect placental microcirculation. Further studies are warranted to determine whether this tool could serve as an early marker of placental function.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 187-192"},"PeriodicalIF":3.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131021","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":"DEHP exposure alters carcinoembryonic antigen family member transcript levels and modulates responses to activin A in the murine placenta","authors":"Lacey Klompmaker ,&nbsp;Sarah C. Moody ,&nbsp;Junlan (Iris) Ma ,&nbsp;Emily J. Camm ,&nbsp;Constance Malliaras ,&nbsp;Sarah A. Marshall ,&nbsp;Kate L. Loveland","doi":"10.1016/j.placenta.2025.05.017","DOIUrl":"10.1016/j.placenta.2025.05.017","url":null,"abstract":"<div><h3>Introduction</h3><div>Activin A affects placental decidualisation and trophoblast growth and invasion. Levels increase during pregnancy, peaking at parturition, while premature elevation is a hallmark of several pregnancy disorders. We examined the impact of unopposed/elevated activin A bioactivity in the inhibin α knockout (<em>Inha</em> KO) mouse placenta which lacks competitive inhibition by inhibin A. We also investigated whether simultaneous exposure to the endocrine disruptor, diethyl-hexyl phthalate (DEHP), which impairs normal placental function and affects activin A signalling in other organs, exacerbates morphological and transcriptional effects.</div></div><div><h3>Methods</h3><div>Litters of <em>Inha</em> WT, Het and KO fetuses were collected at E15.5 from time-mated <em>Inha</em> heterozygous pregnant mice randomly assigned to three groups: untreated, corn oil (Vehicle) or DEHP 500 mg/kg/day, from E12.5–14.5 (n = 2–17). Gross and histological placental morphology was analysed, and bulk RNA-sequencing conducted.</div></div><div><h3>Results</h3><div>Placentae of <em>Inha</em> WT, Het and KO fetuses exhibited no gross morphological differences or differentially expressed genes. However, WT males compared to WT females displayed significantly increased placenta size and labyrinth area. DEHP exposure significantly increased fetal resorption at E15.5 but yielded limited differences in placental morphology. Sex- and genotype-specific transcript alterations in DEHP-exposed placentae included four carcinoembryonic antigen family transcripts (<em>Ceacam13, Gm5155, Psg18, Psg-ps1)</em> and four additional trancripts (<em>Cts3, Ssr4,</em> Sec<em>11c, Taf7l</em>) altered in all genotypes.</div></div><div><h3>Discussion</h3><div>Despite minimal morphological changes, transcriptomic differences suggest that spongiotrophoblast cells and syncytiotrophoblast giant cells are DEHP exposure targets, with carcinoembryonic antigen family transcripts susceptible to its effects. Additionally, DEHP modulates placental gene transcript levels when activin A is unopposed <em>in vivo</em>.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 216-226"},"PeriodicalIF":3.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139111","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":"Presepsin in the amniotic fluid is a useful clinical inflammatory biomarker for the prenatal predictive diagnosis of histologic chorioamnionitis: a retrospective preliminary study","authors":"Masamitsu Kurakazu ,&nbsp;Daichi Urushiyama ,&nbsp;Toyofumi Hirakawa,&nbsp;Fusanori Yotsumoto","doi":"10.1016/j.placenta.2025.05.018","DOIUrl":"10.1016/j.placenta.2025.05.018","url":null,"abstract":"<div><h3>Introduction</h3><div>This study investigated whether presepsin in the amniotic fluid is a useful inflammatory biomarker for the prenatal predictive diagnose of histologic chorioamnionitis (HC).</div></div><div><h3>Methods</h3><div>This retrospective study included 38 singleton pregnant women who were suspected of having an intrauterine infection. All patients underwent amniocentesis and amniotic fluid levels of presepsin (P-SEP), interleukin-8 (IL-8), and interleukin-6 (IL-6) were measured. Concentrations of P-SEP, IL-8, and IL-6 were evaluated for each stage of Blanc's classifications, and correlations between the concentrations were evaluated. Patients were divided into two groups based on the presence or absence of HC and predictors of HC were assessed using a logistic regression model with a combination of maternal white blood cell count (WBC) and maternal C-reactive protein level (CRP) and P-SEP.</div></div><div><h3>Results</h3><div>The concentrations of P-SEP for Blanc's Stage Ⅱ (<em>p</em> = 0.0219) and Stage Ⅲ (<em>p</em> = 0.0262) were significantly higher than those for Blanc's Stage 0. The concentration of P-SEP correlated significantly with that of IL-8 (<em>p</em> = 0.0001) and IL-6 (<em>p</em> &lt; 0.0001). Multivariable analysis showed that WBC (odds ratio (OR), 1.27; 95 % confidence interval (CI), 1.03–1.68), CRP (OR, 1.13; 95 % CI, 0.87–1.58), and P-SEP (OR, 1.12; 95 % CI, 1.00–1.28) were significant predictors of HC.</div></div><div><h3>Discussion</h3><div>P-SEP can be measured in the amniotic fluid and a combination of maternal biomarkers, and P-SEP can predict HC with high accuracy. Therefore, our data provide relevant information to support the early prenatal detection of HC in patients with a suspected intrauterine infection.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 181-186"},"PeriodicalIF":3.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144124194","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":"Genetic background influences susceptibility to exencephaly in Scavenger receptor Class B type 1-deficient mouse embryos.","authors":"Camila Romero-Muñoz, Patricia Romo-Toledo, Gabriela Belledonne, Dolores Busso","doi":"10.1016/j.placenta.2025.05.016","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.016","url":null,"abstract":"<p><strong>Introduction: </strong>Neural tube defects (NTD) are congenital malformations influenced by genetic and environmental factors. Mouse embryos deficient in Scavenger Receptor Class B Type 1 (SR-B1) exhibit female-skewed cranial NTD (exencephaly). This defect is preventable by maternal vitamin E supplementation in a C57BL/6J:129S1/SvImJ (B6:129) 1:1 background. In humans, genetic variability-such as differences across races or ethnic groups-modulates NTD penetrance and severity.</p><p><strong>Aim and methods: </strong>This study compared reproductive outcomes and NTD incidence in two colonies of SR-B1-deficient mice (SR-B1 and SR-B1/J) with shared origin but differing backcrossing histories. The genetic background of each strain was determined using single-nucleotide-polymorphism (SNP)-based sequencing analysis.</p><p><strong>Results: </strong>SR-B1/J mice showed significantly smaller litter sizes, slower development, and higher NTD incidence in SR-B1 KO embryos at gestational day 9.5 (E9.5) compared to SR-B1 mice. SNP analysis revealed a 50 % contribution of the 129 strain in SR-B1 mice versus 80 % in SR-B1/J mice. We also evaluated the preventive effect of maternal vitamin E supplementation in the SR-B1/J colony. Feeding dams a vitamin E-enriched diet reduced NTD incidence in the SR-B1/J colony, consistent with previous findings in the SR-B1 colony.</p><p><strong>Discussion: </strong>This study highlights the critical influence of genetic background on NTD susceptibility in SR-B1 KO mice and demonstrates that vitamin E can reduce NTD risk across different genetic backgrounds. These findings underscore the importance of considering genetic variability in translational research and pave the way for further exploration of genetic modifiers that could enhance our understanding and prevention of NTD.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182459","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}