TGF-β induces Smad2 Phosphorylation, ARE Induction, and Trophoblast Differentiation
International Journal of Stem Cells
;
: 111-120, 2018.
Artículo
en Inglés
| WPRIM
| ID: wpr-739915
ABSTRACT
BACKGROUND:
Transforming growth factor beta (TGF-β) signaling has been shown to control a large number of critical cellular actions such as cell death, differentiation, and development and has been implicated as a major regulator of placental function. SM10 cells are a mouse placental progenitor cell line, which has been previously shown to differentiate into nutrient transporting, labyrinthine-like cells upon treatment with TGF-β. However, the signal transduction pathway activated by TGF-β to induce SM10 progenitor differentiation has yet to be fully investigated. MATERIALS ANDMETHODS:
In this study the SM10 labyrinthine progenitor cell line was used to investigate TGF-β induced differentiation. Activation of the TGF-β pathway and the ability of TGF-β to induce differentiation were investigated by light microscopy, luciferase assays, and Western blot analysis. RESULTS ANDCONCLUSIONS:
In this report, we show that three isoforms of TGF-β have the ability to terminally differentiate SM10 cells, whereas other predominant members of the TGF-β superfamily, Nodal and Activin A, do not. Additionally, we have determined that TGF-β induced Smad2 phosphorylation can be mediated via the ALK-5 receptor with subsequent transactivation of the Activin response element. Our studies identify an important regulatory signaling pathway in SM10 progenitor cells that is involved in labyrinthine trophoblast differentiation.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fosforilación
/
Placenta
/
Células Madre
/
Trofoblastos
/
Transducción de Señal
/
Activación Transcripcional
/
Western Blotting
/
Factor de Crecimiento Transformador beta
/
Muerte Celular
/
Isoformas de Proteínas
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
Idioma:
Inglés
Revista:
International Journal of Stem Cells
Año:
2018
Tipo del documento:
Artículo
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