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早发型和晚发型子痫前期合并妊娠中胎盘细胞外囊泡相关Fas配体和肿瘤坏死因子相关凋亡诱导配体的评估

Assessment of Placental Extracellular Vesicles-Associated Fas Ligand and TNF-Related Apoptosis-Inducing Ligand in Pregnancies Complicated by Early and Late Onset Preeclampsia.

作者信息

Ayala-Ramírez Paola, Machuca-Acevedo Catalina, Gámez Tatiana, Quijano Sandra, Barreto Alfonso, Silva Jaime L, Olaya-C Mercedes, García-Robles Reggie

机构信息

Human Genetics Institute, Faculty of Medicine, Pontificia Universidad Javeriana, Bogotá, Colombia.

Grupo de Inmunobiología y Biología Celular, Unidad de Investigación en Ciencias Biomédicas, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, Colombia.

出版信息

Front Physiol. 2021 Jul 23;12:708824. doi: 10.3389/fphys.2021.708824. eCollection 2021.

Abstract

Preeclampsia (PE) is a hypertensive disorder that affects 2-8% of pregnancies and is one of the main causes of fetal, neonatal, and maternal mortality and morbidity worldwide. Although PE etiology and pathophysiology remain unknown, there is evidence that the hyperactivation of maternal immunity cells against placental cells triggers trophoblast cell apoptosis and death. It has also been reported that placenta-derived extracellular vesicles (EV) carry Fas ligand (FasL) and Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and trigger apoptosis in Jurkat T cells. This study aimed to quantify and compare FasL and TRAIL expression in EV derived from cultures of placenta explants from women with PE (early versus late) and women with uncomplicated pregnancies. Also, the study assessed EV capacity to induce apoptosis in Jurkat T cells. The authors isolated EV from placenta explant cultures, quantified FasL and TRAIL using ELISA, and analyzed EV apoptosis-inducing capability by flow cytometry. Results showed increased FasL and TRAIL in EV derived from placenta of women with PE, and increased EV apoptosis-inducing capability in Jurkat T cells. These results offer supporting evidence that EV FasL and TRAIL play a role in the pathophysiology of PE.

摘要

子痫前期(PE)是一种高血压疾病,影响2%-8%的妊娠,是全球范围内胎儿、新生儿及孕产妇死亡和发病的主要原因之一。尽管PE的病因和病理生理学尚不清楚,但有证据表明,母体免疫细胞针对胎盘细胞的过度激活会引发滋养层细胞凋亡和死亡。也有报道称,胎盘来源的细胞外囊泡(EV)携带Fas配体(FasL)和肿瘤坏死因子相关凋亡诱导配体(TRAIL),并触发Jurkat T细胞凋亡。本研究旨在定量和比较PE患者(早期与晚期)和正常妊娠女性胎盘外植体培养物来源的EV中FasL和TRAIL的表达。此外,该研究评估了EV诱导Jurkat T细胞凋亡的能力。作者从胎盘外植体培养物中分离出EV,使用酶联免疫吸附测定法(ELISA)对FasL和TRAIL进行定量,并通过流式细胞术分析EV的凋亡诱导能力。结果显示,PE患者胎盘来源的EV中FasL和TRAIL增加,Jurkat T细胞中EV的凋亡诱导能力增强。这些结果为EV FasL和TRAIL在PE病理生理学中发挥作用提供了支持证据。

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