Smad3-dependent nuclear translocation of beta-catenin is required for TGF-beta1-induced proliferation of bone marrow-derived adult human mesenchymal stem cells.
Adult mesenchymal stem cells (MSCs) derived from bone marrow contribute to the regeneration of multiple types of mesenchymal tissues. Here we describe the functional role of a novel form of cross-talk between the transforming growth factor beta1 (TGF-beta1) and Wnt signaling pathways in regulating the activities of human MSCs. We show that TGF-beta1 induces rapid nuclear translocation of beta-catenin in MSCs in a Smad3-dependent manner. Functionally, this pathway is required for the stimulation of MSC proliferation and the inhibition of MSC osteogenic differentiation by TGF-beta1, likely through the regulation of specific downstream target genes. These results provide evidence for a new mode of cooperation between the TGF-beta and Wnt signaling pathways in this specific cellular context and suggest a potentially important role for this distinct signaling pathway in the control of self-renewal and differentiation of a specific type of MSCs.
Duke Scholars
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Related Subject Headings
- beta Catenin
- Wnt Proteins
- Transforming Growth Factor beta
- Smad3 Protein
- Signal Transduction
- Reverse Transcriptase Polymerase Chain Reaction
- Protein Transport
- Mesenchymal Stem Cells
- Humans
- Developmental Biology
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- beta Catenin
- Wnt Proteins
- Transforming Growth Factor beta
- Smad3 Protein
- Signal Transduction
- Reverse Transcriptase Polymerase Chain Reaction
- Protein Transport
- Mesenchymal Stem Cells
- Humans
- Developmental Biology