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A mesenchymal-to-epithelial transition initiates and is required for the nuclear reprogramming of mouse fibroblasts.

Abstract：

:Epithelial-to-mesenchymal transition (EMT) is a developmental process important for cell fate determination. Fibroblasts, a product of EMT, can be reset into induced pluripotent stem cells (iPSCs) via exogenous transcription factors but the underlying mechanism is unclear. Here we show that the generation of iPSCs from mouse fibroblasts requires a mesenchymal-to-epithelial transition (MET) orchestrated by suppressing pro-EMT signals from the culture medium and activating an epithelial program inside the cells. At the transcriptional level, Sox2/Oct4 suppress the EMT mediator Snail, c-Myc downregulates TGF-beta1 and TGF-beta receptor 2, and Klf4 induces epithelial genes including E-cadherin. Blocking MET impairs the reprogramming of fibroblasts whereas preventing EMT in epithelial cells cultured with serum can produce iPSCs without Klf4 and c-Myc. Our work not only establishes MET as a key cellular mechanism toward induced pluripotency, but also demonstrates iPSC generation as a cooperative process between the defined factors and the extracellular milieu. PAPERCLIP:

journal_name

Cell Stem Cell

journal_title

Cell stem cell

authors

Li R,Liang J,Ni S,Zhou T,Qing X,Li H,He W,Chen J,Li F,Zhuang Q,Qin B,Xu J,Li W,Yang J,Gan Y,Qin D,Feng S,Song H,Yang D,Zhang B,Zeng L,Lai L,Esteban MA,Pei D

doi

10.1016/j.stem.2010.04.014

subject

Has Abstract

pub_date

2010-07-02 00:00:00

pages

51-63

issue

1

eissn

1934-5909

issn

1875-9777

pii

S1934-5909(10)00169-4

journal_volume

7

pub_type

杂志文章

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