Journal
ONCOGENE
Volume 32, Issue 28, Pages 3381-3389Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2012.342
Keywords
Snail1; mesenchymal stem cells; TGF-beta; Akt
Funding
- la Fundacion Cientifica de la Asociacion Espanola contra el Cancer
- Ministerio de Ciencia y Tecnologia [SAF2006-00339, SAF2010-16089]
- Fundacio La Marato de TV3
- NIH [R01HD034883]
- ISCIII/FEDER [RD06/0020/0109, RD06/0020/0040, RD06/0020/0020]
- Generalitat de Catalunya [2009SGR867]
- FPI
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The Snail1 transcriptional repressor plays a key role in triggering epithelial-to-mesenchymal transition. Although Snail1 is widely expressed in early development, in adult animals it is limited to a subset of mesenchymal cells where it has a largely unknown function. Using a mouse model with inducible depletion of Snail1, here we demonstrate that Snail1 is required to maintain mesenchymal stem cells (MSCs). This effect is associated to the responsiveness to transforming growth factor (TGF)-beta 1 that shows a strong Snail1 dependence. Snail1 depletion in conditional knockout adult animals causes a significant decrease in the number of bone marrow-derived MSCs. In culture, Snail1-deficient MSCs prematurely differentiate to osteoblasts or adipocytes and, in contrast to controls, are resistant to the TGF-beta 1-induced differentiation block. These results demonstrate a new role for Snail1 in TGF-beta response and MSC maintenance.
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