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TGF- β induces Smad2 Phosphorylation, ARE Induction, and Trophoblast Differentiation.
International Journal of Stem Cells 2018 May 31
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 and Methods: 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 and Conclusions: 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.
Materials and Methods: 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 and Conclusions: 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.
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