Placenta最新文献

{"title":"Effects of semen inflammation on embryo implantation, placentation, pregnancy outcomes and offspring health.","authors":"María S Martinez, Yair A Chocobar, Yamila Fariz, Daniela A Paira, Virginia E Rivero, Rubén D Motrich","doi":"10.1016/j.placenta.2025.02.002","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.02.002","url":null,"abstract":"<p><p>This review explores the critical role of semen inflammation in sperm quality, embryo implantation, placentation, and its broader implications on reproductive health. Chronic inflammation of the male genital tract has been increasingly recognized as a significant factor contributing to infertility. This inflammation not only impairs semen quality but also disrupts the intricate immune cross-talk between the male and female genital tracts, which is essential for successful implantation, placentation and pregnancy. The review synthesizes existing research on the mechanisms by which inflammatory mediators in semen influence the female immune environment, leading to altered uterine receptivity, placental formation, and embryo implantation. Furthermore, the impact of these disruptions on the health and development of the offspring is discussed, highlighting the transgenerational effects of male genital tract inflammation. Through an examination of both animal models and human studies, this review underscores the need for a deeper understanding of the immune interactions in reproductive biology and the potential for novel therapeutic interventions aimed at mitigating the adverse outcomes associated with semen inflammation.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409918","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":"Nitrative stress-induced dysregulation of placental AQUAPORIN-9: A potential key player in preeclampsia pathogenesis.","authors":"Yollyseth Medina, Nazarena Fernandez, Matías N Sierra, Mauricio Castro Parodi, Alicia E Damiano","doi":"10.1016/j.placenta.2025.02.001","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.02.001","url":null,"abstract":"<p><p>Preeclampsia is associated with increased oxidative and nitrative stress, resulting in elevated protein nitration and potential functional impairment. Previously, we found an increased expression of AQP9 protein with a loss of function in preeclamptic placentas. However, the link between nitrative stress and AQP9 has not yet been explored. Here, we aimed to evaluate the effect of nitrative stress on placental AQP9 and its role in the pathogenesis of preeclampsia. In silico analysis was conducted on the amino acid sequences of AQP9 to identify potential nitration sites. Levels of 3NyT-AQP9 were assessed by immunoprecipitation in normal and preeclamptic placentas. AQP9 expression and function were evaluated by culturing normal placental explants with 0, 25, 50, 100, and 200 μM ONOO- to induce nitrative stress. Viability and integrity of the explants and stress markers were determined. Water uptake and utilization of lactate mediated by AQP9 were studied along with the molecular expression of AQP9 and 3-NyT-AQP9. The in silico analysis showed that AQP9 is more susceptible to nitration than other AQPs. The abundance of nitrated AQP9 significantly increased in preeclamptic placentas compared to normal ones (n = 4; p < 0.05). Peroxynitrite treatment also increased AQP9 protein expression without altering its gene expression and impaired the transport of water and lactate mediated by this protein. Our findings provide evidence that nitrative stress induces the nitration of AQP9 protein, leading to the accumulation of a non-functional protein in the syncytiotrophoblasts. Therefore, this altered protein may play a pivotal role in the pathogenesis of preeclampsia by disrupting cellular homeostasis.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425904","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 SMEK1 regulates trophoblast migration and invasion in fetal growth restriction","authors":"Anna Li ,&nbsp;Man Zhao ,&nbsp;Ziming Lin ,&nbsp;Zexin Yang ,&nbsp;Pihai Gong ,&nbsp;Chunying Wang ,&nbsp;Zhenya Fang ,&nbsp;Meihua Zhang","doi":"10.1016/j.placenta.2025.02.005","DOIUrl":"10.1016/j.placenta.2025.02.005","url":null,"abstract":"<div><h3>Introduction</h3><div>Fetal growth restriction (FGR) is a significant pregnancy condition characterized by the fetus failing to attain its full genetic growth potential. FGR is primarily ascribed to defective placentation, owing to impaired trophoblast cellular function. The objective of this research is to elucidate the pathogenic functions of suppressor of Mek1 (SMEK1) in FGR.</div></div><div><h3>Methods</h3><div>Western blot and Immunofluorescence were used to detect the expression and localization of SMEK1 in placenta. We overexpressed and knocked down SMEK1 using plasmid or siRNA special targeted it. EdU Assay, flow cytometry, Western blot, Wound healing migration and Transwell insert assay were used to detect the influence of SMEK1 on cellular function. The mechanism of SMEK1 in regulating the migration of JEG3 cells was predicted by employing transcriptomics and bioinformatics analysis, and was validated by Western blot.</div></div><div><h3>Results</h3><div>The expression of SMEK1 was downregulated in FGR placentas. The aberrant expression of SMEK1 in JEG3 cells is associated with cell migration and invasion, but not with proliferation, or apoptosis. Transcriptomic analysis and Western blots indicate that knockdown of SMEK1 inhibited the PI3K/Akt/mTOR pathway. A significant inhibition was observed in the epithelial-mesenchymal transition (EMT) process of JEG3 cells within the SMEK1 knockdown group. The activation of the PI3K/Akt/mTOR pathway partially restored the impaired migration and invasive ability due to SMEK1 knockdown in JEG3 cells.</div></div><div><h3>Discussion</h3><div>the reduction of SMEK1 may contribute to the development of FGR by hindering the EMT process of trophoblast cells through modulation of the PI3K/Akt/mTOR signaling pathway.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"161 ","pages":"Pages 65-75"},"PeriodicalIF":3.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377041","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":"Consequences of the modulation of gestational resistance training intensity for placental cell composition and nutrient transporter expression","authors":"Thaynan Raquel dos Prazeres Oliveira ,&nbsp;Débora Priscila Lima-Oliveira ,&nbsp;Maira Beatriz Matos de Paula ,&nbsp;Rafael Victor Lira Brito ,&nbsp;Alvaro Nascimento Barreto ,&nbsp;Alluanan Adelson do Nascimento Silva ,&nbsp;Fernanda Carolina Ribeiro Dias ,&nbsp;Valdemiro Amaro da Silva-Junior ,&nbsp;Osmar Henrique Dos Santos-Junior ,&nbsp;Claudia Jacques Lagranha ,&nbsp;Kelli Nogueira Ferraz-Pereira ,&nbsp;José Antonio-Santos ,&nbsp;Raquel Da Silva Aragão","doi":"10.1016/j.placenta.2025.01.012","DOIUrl":"10.1016/j.placenta.2025.01.012","url":null,"abstract":"<div><h3>Introduction</h3><div>Resistance training during pregnancy provides benefits for the mother and fetus, but little is known about the effects of resistance training on placental structure and function or the repercussions of modifying resistance training intensity on the mother-fetus-placenta triad.</div></div><div><h3>Methods</h3><div>Female Wistar rats were submitted to resistance training involving a ladder climb (80 % of maximum load carried (MLC), 5-day/week for 3-weeks) before pregnancy. After confirmation of mating, the rats were randomly divided into three groups, according to resistance training intensity during pregnancy: constant-intensity training (CIT, trained at 80 % of MLC through gestation), decreasing-intensity training (DIT, 80 % of MLC during first and second weeks of gestation and 50 % of MLC in the third week), and undulating-intensity training (UIT, 50 % of MLC in the first and third weeks, and 80 % of MLC in the second week). A control group did not undergo any training. Samples were collected on gestational day 20.</div></div><div><h3>Results</h3><div>Resistance training had no impact on maternal body weight, muscle glycogen content, adipocyte morphology, number of fetuses, number of absorptions, placental area, or fetal growth parameters. The CIT group presented lower maternal serum glucose. The UIT group presented increased presence of fetal capillaries in the labyrinth zone and increased <em>Glut1</em>, <em>Glut3</em>, and <em>Snat1</em> expression in the placenta. <em>Snat2</em> expression was upregulated in all resistance training groups and higher levels of <em>Mtor</em> expression were found in the DIT group. <em>Il1b</em> expression increased in the CIT group, and higher levels of <em>Il10</em> expression were found in the DIT and UIT groups.</div></div><div><h3>Discussion</h3><div>Resistance training was safe for pregnant rats. Its influence on glucose and amino acid transport was not dependent on changes in <em>Mtor</em> expression and did not impact fetal growth.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"161 ","pages":"Pages 55-64"},"PeriodicalIF":3.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143232089","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":"Ferumoxytol-enhanced MRI of retroplacental clear space disruption in placenta accreta spectrum","authors":"Andrew A. Badachhape ,&nbsp;Brian Burnett ,&nbsp;Prajwal Bhandari ,&nbsp;Laxman Devkota ,&nbsp;Rohan Bhavane ,&nbsp;Renuka Menon ,&nbsp;Mayank Srivastava ,&nbsp;Hennie Lombaard ,&nbsp;Amir Shamshirsaz ,&nbsp;Ketan B. Ghaghada ,&nbsp;Karin A. Fox ,&nbsp;Ananth V. Annapragada","doi":"10.1016/j.placenta.2024.12.026","DOIUrl":"10.1016/j.placenta.2024.12.026","url":null,"abstract":"<div><h3>Introduction</h3><div>Placenta accreta spectrum (PAS) occurs when the placenta is pathologically adherent to the myometrium. An intact retroplacental clear space (RPCS) is a marker of normal placentation. In this study, we investigate use of the FDA-approved iron supplement ferumoxytol for contrast-enhanced MRI of the RPCS in mouse models of normal pregnancy and PAS. We then demonstrate the translational potential of this technique in human patients (n = 6) presenting with severe PAS (FIGO Grade 3C), moderate PAS (FIGO Grade 1), and no PAS.</div></div><div><h3>Methods</h3><div>T1-weighted sequences were used to determine the optimal dose of ferumoxytol in pregnant mice. Pregnant Gab3^−/− mice which demonstrate adherent placentation were imaged alongside wild-type (WT) pregnant mice with non-adherent placentation. Fe-MRI was also performed in 6 pregnant subjects using standard T1 and T2 weighted sequences and a 3D magnetic resonance angiography (MRA) sequence.</div></div><div><h3>Results</h3><div>Ferumoxytol administered at 5 mg/kg led to strong placental enhancement in Fe-MRI images. Gab3^−/− mice demonstrated loss of the hypointense region characteristic of the RPCS relative to WT mice. In human patients, Fe-MRI enabled high uteroplacental vasculature signal and quantification of the volume and signal profile in severe and moderate invasion of the placenta relative to non-PAS cases.</div></div><div><h3>Discussion</h3><div>Ferumoxytol, an FDA-approved iron oxide nanoparticle formulation, enabled T1w MRI visualization of abnormal vascularization and loss of uteroplacental interface in a murine model of PAS. The potential of this non-invasive visualization technique was then further demonstrated in human subjects and suggests the possibility of PAS diagnosis using contrast enhanced MRI.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 100-106"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142953793","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 relationship between abnormal fetoplacental Dopplers, angiogenic markers of placental dysfunction and adverse perinatal outcomes in diabetic pregnancies with small fetuses – A prospective study","authors":"Jesrine Hong ,&nbsp;Kylie Crawford ,&nbsp;Erika Cavanagh ,&nbsp;Vicki Clifton ,&nbsp;Fabricio da Silva Costa ,&nbsp;Anthony V. Perkins ,&nbsp;Sailesh Kumar","doi":"10.1016/j.placenta.2024.12.025","DOIUrl":"10.1016/j.placenta.2024.12.025","url":null,"abstract":"<div><h3>Introduction</h3><div>The aim of this study was to evaluate differences in circulating maternal placental biomarkers and fetoplacental Dopplers in women with diabetes mellitus in pregnancy (DIP) with prenatally identified small fetuses (defined as &lt;20th centile for gestational age) compared to women with small fetuses without DIP.</div></div><div><h3>Methods</h3><div>This was a prospective cohort study of women with DIP with small infants compared to a non-diabetic cohort with similarly small fetuses. Multivariable logistic regression was used to evaluate the effect of DIP on placental biomarkers, fetoplacental Dopplers, and adverse perinatal outcomes.</div></div><div><h3>Results</h3><div>There were 447 pregnancies in this study – 117 (26.2 %) had DIP and 330 (73.8 %) did not have diabetes. Of the DIP cohort, 57 (48.7 %) had early-onset and 27 (23.1 %) had late-onset FGR. Higher rates of low PlGF levels&lt;100 ng/L (42.1 % vs. 25.7 %,p = 0.002), high sFlt-1/PlGF ratio (39.6 % vs. 25.4 %,p = 0.006), low MCA PI &lt; 5th centile at recruitment (18.8 % vs. 7.6 %,p &lt; 0.001, OR 2.37 95%CI 1.25, 4.46,p = 0.008), abnormal UA Doppler before delivery (OR 1.63 95%CI 1.00, 2.66,p = 0.048) were seen in the DIP cohort. DIP was associated with higher rates of emergency cesarean section (43.6 % vs. 26.7 %,p = 0.001) and lower birthweight (2300 (1558, 2610g) vs. 2447 (2050, 2690g),p = 0.003). The odds of early FGR (OR 1.90 95%CI 1.20, 2.98,p = 0.006), PTB&lt;37 weeks (OR 1.66 95%CI 1.02, 2.70,p = 0.039), PTB&lt;34 weeks’ gestation (OR 3.00 95%CI 1.51, 5.96,p = 0.002), composite non-neurological neonatal morbidity (OR 1.86 95%CI 1.04, 3.33,p = 0.037), and hypoglycemia (OR 3.69 95%CI 1.59, 8.54,p = 0.002) were significantly higher in DIP.</div></div><div><h3>Conclusions</h3><div>DIP is associated with increased risks of early-onset FGR, PTB, composite severe non-neurological neonatal morbidity, and neonatal hypoglycemia in women with small infants. DIP was significantly associated with increased odds of MCA PI &lt; 5th centile at diagnosis and abnormal UA Doppler before birth.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Pages 51-59"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143158296","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 vascularized 3d placenta-on-a-chip to study barrier dysfunction in pre-eclampsia","authors":"Marta Cherubini ,&nbsp;Defne Cobanoglu ,&nbsp;Kristina Haase","doi":"10.1016/j.placenta.2024.10.045","DOIUrl":"10.1016/j.placenta.2024.10.045","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":"143376801","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":"“GPI signal lost”: Implications for preeclampsia","authors":"Andrea Álvarez-Sánchez ,&nbsp;Johanna Grinat ,&nbsp;Paula Doria-Borrell ,&nbsp;Marta Malenchini ,&nbsp;Maravillas Mellado-López ,&nbsp;Salvador Meseguer ,&nbsp;Myriam Hemberger ,&nbsp;Vicente Pérez-García","doi":"10.1016/j.placenta.2024.10.043","DOIUrl":"10.1016/j.placenta.2024.10.043","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 149"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143375843","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 role of xanthine oxidase in pregnancy’s outcomes","authors":"Lorenzo Annesi ,&nbsp;Giovanni Tossetta ,&nbsp;Claudio Borghi ,&nbsp;Federica Piani","doi":"10.1016/j.placenta.2024.10.064","DOIUrl":"10.1016/j.placenta.2024.10.064","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 156"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143375844","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":"HAPLN3 is involved in trophoblast differentiation and invasion","authors":"Ana Ferrero-Micó ,&nbsp;Sergio Navarro-Serna ,&nbsp;Paula Doria-Borrell ,&nbsp;Maravillas Mellado-López ,&nbsp;Vicente Pérez-García","doi":"10.1016/j.placenta.2024.10.052","DOIUrl":"10.1016/j.placenta.2024.10.052","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"160 ","pages":"Page 152"},"PeriodicalIF":3.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143376745","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}