FGF-2 acts through an ERK1/2 intracellular pathway to affect osteoblast differentiation. Academic Article uri icon

Overview

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.

authors

  • Spector, Jason A.
  • Mathy, Jonathan A
  • Warren, Stephen M
  • Nacamuli, Randall P
  • Song, Hanjoon M
  • Lenton, Kelly
  • Fong, Kenton D
  • Fang, Dongyu T
  • Longaker, Michael T

publication date

  • March 1, 2005

Research

keywords

  • Bone Morphogenetic Proteins
  • Cell Differentiation
  • DNA-Binding Proteins
  • Extracellular Signal-Regulated MAP Kinases
  • Fibroblast Growth Factor 2
  • Homeodomain Proteins
  • Osteoblasts
  • Transforming Growth Factor beta

Identity

Scopus Document Identifier

  • 14644445116

Digital Object Identifier (DOI)

  • 10.1097/01.prs.0000153035.73507.7b

PubMed ID

  • 15731686

Additional Document Info

volume

  • 115

issue

  • 3