Assessment of placental extracellular vesicles-associated fas ligand and TNF-related apoptosis-inducing ligand in pregnancies complicated by early and late onset preeclampsia

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 cel...

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Autores:
Ayala Ramírez, Paola
Machuca-Acevedo, Catalina
Gámez, Tatiana
Quijano Gómez, Sandra Milena
Barreto Prieto, Alfonso
Silva Herrera, Jaime Luis
Olaya Contreras, Mercedes
García-Robles, Reggie
Rivatrem
Tipo de recurso:
Article of investigation
Fecha de publicación:
2021
Institución:
Pontificia Universidad Javeriana
Repositorio:
Repositorio Universidad Javeriana
Idioma:
OAI Identifier:
oai:repository.javeriana.edu.co:10554/60055
Acceso en línea:
https://www.frontiersin.org/articles/10.3389/fphys.2021.708824/full
http://hdl.handle.net/10554/60055
https://doi.org/10.3389/fphys.2021.708824
Palabra clave:
Pregnancy
Hypertension Disorder Complicating Pregnancy
Exosome (Vesicle)
Apoptosis
Placental Culture
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License
Atribución-NoComercial 4.0 Internacional
Description
Summary: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 apoptosisinducing 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.