Background: Bone defect caused by trauma, tumor resection, infection or
congenital malformation is a common clinical disease. Bone tissue engineering is
regarded as a promising way of bone defect reconstruction. Thus, agents that can
promote osteogenesis have received great attention. Cytochalasin D (Cyto D), a
metabolite derived from molds, proves to be able to modify actin, reorganize
cytoskeleton, and then promote the osteogenic differentiation.
Objective: The purpose of this study was to explore the effect and mechanism of Cyto
D on osteogenic differentiation of mouse pre-osteoblast MC3T3-E1 cells.
Methods: The optimum concentration of Cyto D was explored. The osteogenic
differentiation of MC3T3-E1 cells induced by Cyto D was assessed by alkaline
phosphatase (ALP) staining, Alizarin Red S (ARS) staining, western blotting and
quantitative real-time polymerase chain reaction (RT-qPCR). In addition, a specific
pathway inhibitor was utilized to explore whether MAPK pathways were involved in this
Results: The results showed that the optimized concentration of action was 10-2µg/ml.
The expression of Runx2, OCN and OSX was up-regulated by the supplement of Cyto
D. ALP activity, calcium deposition, and phosphorylation level of p38 protein were also
improved. Inhibition of the pathway significantly reduced the activation of p38, and the
expression of osteogenic-related genes.
Conclusion: Cyto D can promote the osteogenic differentiation of MC3T3 cells via the
p38-MAPK signaling pathway, but not the ERK1/2 or JNK, and it is a potential agent to
improve the osteogenesis of MC3T3 cells.