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FGF-2 acts through an ERK1/2 intracellular pathway to affect osteoblast differentiation PLASTIC AND RECONSTRUCTIVE SURGERY Spector, J. A., Mathy, J. A., Warren, S. M., Nacamuli, R. P., Song, H. M., Lenton, K., Fong, K. D., Fang, D. T., Longaker, M. T. 2005; 115 (3): 838-852

Abstract

An abundance of genetic and experimental data have suggested that fibroblast growth factor (FGF) signaling plays a central role in physiological and pathological cranial suture fusion. Although alterations in the differentiation and proliferation of sutural osteoblasts may be a key mediator of this process, the mechanisms by which FGF signaling regulates osteoblast differentiation remain incompletely understood. In the current study, the authors show that recombinant human FGF-2 alters osteoblastic expression of bone morphogenetic protein-2 and Msx-2 in vitro to favor cellular differentiation and osteoinduction. The ERK1/2 intracellular signaling cascade was shown to be necessary for recombinant human FGF-2-mediated bone morphogenetic protein-2 transcriptional changes. Furthermore, the cellular production of an intermediate transcriptional modifier was found to be necessary for the recombinant human FGF-2-mediated gene expression changes in bone morphogenetic protein-2 and Msx-2. Together, these findings offer new insight into the mechanisms by which FGF-2 modulates osteoblast biology.

View details for DOI 10.1097/01.PRS.0000153035.73507.7B

View details for Web of Science ID 000227432100023

View details for PubMedID 15731686