Zusammenfassung
Objective: Dental follicle cells (DFCs) are the genuine precursors of alveolar osteoblasts. Previous studies suggested that collagen I supports the osteogenic differentiation of DFCs. This study investigated the effect of collagen I on the osteogenic differentiation of human DFCs. Materials and methods: We modified the cell culture surface with collagen I and evaluated the osteogenic ...
Zusammenfassung
Objective: Dental follicle cells (DFCs) are the genuine precursors of alveolar osteoblasts. Previous studies suggested that collagen I supports the osteogenic differentiation of DFCs. This study investigated the effect of collagen I on the osteogenic differentiation of human DFCs. Materials and methods: We modified the cell culture surface with collagen I and evaluated the osteogenic differentiation of DFCs by the gene expression of alkaline phosphatase (ALP) and osteopontin (OPN) and by the assessment of the ALP-activity and Alizarin red staining. FAK and ERK signalling pathways regulation were investigated by Western blot analyses. Cell culture media were supplemented with specific inhibitors of FAK (PF573228) or ERK signalling pathways (PD98059). Results: During the osteogenic differentiation collagen I induced the ALP activity and the expression of the late osteogenic differentiation markers OPN, but it did not stimulate mineralization. The FAK/ERK signalling pathway was activated on collagen I and after the induction of osteogenic differentiation. The inhibition of FAK repressed also the activation of ERK signalling in DFCs and the expression of osteogenic markers ALP and OPN on standard cell culture dishes. After cultivation on collagen I, however, the inhibition of ERK was slightly reverted in DFCs. Here, the expression of OPN was restored, while the expression of ALP was still repressed. Interestingly, the expression of OPN was repressed after the inhibition of ERIC signalling. Conclusion: Collagen I induced independently the expression of the osteogenic differentiation markers ALP and OPN via the FAK and ERIC signalling pathways, respectively. (C) 2014 Elsevier Ltd. All rights reserved.
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