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  Fibroblast growth factor 2 modulates transforming growth factor ß signaling in mouse embryonic fibroblasts and human ESCs (hESCs) to support hESC self-renewal

Greber, B., Lehrach, H., & Adjaye, J. (2006). Fibroblast growth factor 2 modulates transforming growth factor ß signaling in mouse embryonic fibroblasts and human ESCs (hESCs) to support hESC self-renewal. Stem Cells, Stem Cells Express, epub-epub. doi:10.1634/stemcells.2006-0476.

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 Creators:
Greber, Boris1, Author
Lehrach, Hans2, Author           
Adjaye, James3, Author           
Affiliations:
1Max Planck Society, ou_persistent13              
2Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              
3Molecular Embryology and Aging (James Adjaye), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479654              

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 Abstract: Fibroblast growth factor 2 (FGF2) is known to promote self-renewal of human embryonic stem cells (hESCs). In addition, it has been shown that transforming growth factor ß (TGFß) signaling is crucial in that the TGFß/Activin/Nodal branch of the pathway needs to be activated and the bone morphogenic protein (BMP)/GDF branch repressed to prevent differentiation. This holds particularly true for Serum Replacement-based medium containing BMP-like activity. We have reinvestigated a widely used protocol for conditioning hESC medium with mouse embryonic fibroblasts (MEFs). We show that FGF2 acts on MEFs to release supportive factors and reduce differentiation-inducing activity. FGF2 stimulation experiments with supportive and nonsupportive MEFs followed by genome-wide expression profiling revealed that FGF2 regulates the expression of key members of the TGFß pathway, with Inhba, Tgfb1, Grem1, and Bmp4 being the most likely candidates orchestrating the above activities. In addition, restimulation experiments in hESCs combined with global expression analysis revealed downstream targets of FGF2 signaling in these cells. Among these were the same factors previously identified in MEFs, thus suggesting that FGF2, at least in part, promotes self-renewal of hESCs by modulating the expression of TGFß ligands, which, in turn, act on hESCs in a concerted and autocrine manner.

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Language(s): eng - English
 Dates: 2006-10-12
 Publication Status: Issued
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 Identifiers: eDoc: 307621
DOI: 10.1634/stemcells.2006-0476
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Title: Stem Cells
Source Genre: Journal
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Pages: - Volume / Issue: Stem Cells Express Sequence Number: - Start / End Page: epub - epub Identifier: ISSN: 1066-5099