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Artículo

Leptin promotes HLA-G expression on placental trophoblasts via the MEK/Erk and PI3K signaling pathways

Barrientos, Gabriela LauraIcon ; Toro, Ayelen RayenIcon ; Monschanski, P; Cohen, M.; García, Mariana GabrielaIcon ; Rose, M.; Maskin, Bernardo; Sanchez Margalet, V.; Blois, Sandra M.; Varone, Cecilia LauraIcon
Fecha de publicación: 04/2015
Editorial: W B Saunders Co Ltd
Revista: Placenta
ISSN: 0143-4004
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Otras Ciencias Biológicas

Resumen

Introduction: The development of the human haemochorial placenta requires complex regulatory mechanisms to protect invasive trophoblast cells from cytotoxic responses elicited by maternal immune cells. Leptin, the adipocyte derived hormone encoded by the Lep gene, is synthesized by placental trophoblasts and exerts pleiotropic effects on the immune system, including the promotion of inflammation and the activation of T cell responses. Methods: To address its possible involvement in the modulation of maternal immune responses during pregnancy, we investigated the effect of leptin on the expression of the class Ib histocompatibility antigen HLA-G as one of the chief immunosuppressive strategies used by trophoblast cells. Results: In vitro incubation of the trophoblast derived Swan 71 and JEG-3 cell lines with 25-50 ng/ml recombinant leptin significantly boosted HLA-G mRNA and protein expression, and this effect was abrogated upon pharmacological inhibition of the PI3K-Akt and MEK-Erk signaling pathways. A similar stimulatory effect of leptin was observed in term placental tissue explants, though 10-fold higher doses were required for stimulation. Further, JEG-3 cells treated with a leptin antisense oligodeoxynucleotide displayed decreased HLA-G expression levels, which were partially recovered by addition of stimulating doses of exogenous hormone. Immunofluorescence and qPCR analysis confirmed leptin biosynthesis in placental tissue, further showing that invasive extravillous trophoblast cells were a main source of this hormone during the first trimester of normal pregnancies. Discussion: Taken together, our results show that leptin acts as an autocrine/paracrine signal promoting HLA-G expression in placental trophoblasts suggesting an important role in the regulation of immune evasion mechanisms at the fetal maternal interface.
Palabras clave: Hla-G , Leptin , Placenta , Signal Transduction
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/46904
URL: http://www.placentajournal.org/article/S0143-4004%2815%2900036-3/abstract
DOI: http://dx.doi.org/10.1016/j.placenta.2015.01.006
URL: https://www.sciencedirect.com/science/article/pii/S0143400415000363
Colecciones
Articulos(IQUIBICEN)
Articulos de INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CS. EXACTAS Y NATURALES
Articulos(SEDE CENTRAL)
Articulos de SEDE CENTRAL
Citación
Barrientos, Gabriela Laura; Toro, Ayelen Rayen; Monschanski, P; Cohen, M.; García, Mariana Gabriela; et al.; Leptin promotes HLA-G expression on placental trophoblasts via the MEK/Erk and PI3K signaling pathways; W B Saunders Co Ltd; Placenta; 36; 4; 4-2015; 419-426
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