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Basic fibroblast growth factor inhibits osteogenic differentiation of stem cells from human exfoliated deciduous teeth through ERK signaling
Author(s) -
Li B,
Qu C,
Chen C,
Liu Y,
Akiyama K,
Yang R,
Chen F,
Zhao Y,
Shi S
Publication year - 2012
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2011.01878.x
Subject(s) - basic fibroblast growth factor , fibroblast growth factor , microbiology and biotechnology , mapk/erk pathway , wnt signaling pathway , osteocalcin , signal transduction , biology , stem cell , cellular differentiation , growth factor , chemistry , alkaline phosphatase , biochemistry , receptor , gene , enzyme
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.