Basic fibroblast growth factor inhibits osteogenic differentiation of stem cells from human exfoliated deciduous teeth through ERK signaling
Article first published online: 12 DEC 2011
© 2011 John Wiley & Sons A/S
Volume 18, Issue 3, pages 285–292, April 2012
How to Cite
Li, B., Qu, C., Chen, C., Liu, Y., Akiyama, K., Yang, R., Chen, F., Zhao, Y. and Shi, S. (2012), Basic fibroblast growth factor inhibits osteogenic differentiation of stem cells from human exfoliated deciduous teeth through ERK signaling. Oral Diseases, 18: 285–292. doi: 10.1111/j.1601-0825.2011.01878.x
- Issue published online: 2 MAR 2012
- Article first published online: 12 DEC 2011
- Accepted manuscript online: 21 NOV 2011 10:39AM EST
- Received 23 June 2011; revised 12 October 2011; accepted 2 November 2011
- tissue regeneration
Oral Diseases (2012) 18, 285–292
Objective: Stem cells from human exfoliated deciduous teeth (SHED) are a unique postnatal stem cell population capable of regenerating mineralized tissue and treating immune disorders. However, the mechanism that controls SHED differentiation is not fully understood. Here, we showed that basic fibroblast growth factor (bFGF) treatment attenuated SHED-mediated mineralized tissue regeneration through activation of the extracellular signal-regulated kinase (ERK) 1/2 pathway.
Material and Method: The level of mineralized nodule formation was assessed by alizarin red staining. Expression levels of osteogenic genes, osteocalcin and runt-related transcription factor 2, were examined by RT-PCR. Subcutaneous implantation approach was used to assess in vivo bone formation. Downstream signaling pathways of bFGF were examined by Western blotting.
Result: Activation of ERK1/2 signaling by bFGF treatment inhibited WNT/β-catenin pathway, leading to osteogenic deficiency of SHED. ERK1/2 inhibitor treatment rescued bFGF-induced osteogenic differentiation deficiency.
Conclusion: These data suggest that bFGF inhibits osteogenic differentiation of SHED via ERK1/2 pathway. Blockade ERK1/2 signaling by small molecular inhibitor treatment improves bone formation of SHED after bFGF treatment.