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1: Matrix Biol. 2005 Dec;24(8):520-9. Epub 2005 Oct 25.

FGF upregulates osteopontin in epiphyseal growth plate chondrocytes: implications
for endochondral ossification.

Weizmann S, Tong A, Reich A, Genina O, Yayon A, Monsonego-Ornan E.

Institute of Animal Science, the Volcani Center, Bet Dagan 50250, Israel.

Fibroblast growth factor receptor 3 (FGFR3) signaling pathways are essential for 
normal longitudinal bone growth. Mutations in this receptor lead to various human
growth disorders, including Achondroplasia, disproportionately short-limbed
dwarfism, characterized by narrowing of the hypertrophic region of the epiphyseal
growth plates. Here we find that FGF9, a preferred ligand for FGFR3 rapidly
induces the upregulation and secretion of the matrix resident phosphoprotein,
osteopontin (OPN) in cultured chicken chondrocytes. This effect was observed as
early as two hours post stimulation and at FGF9 concentrations as low as 1.25
ng/ml at both mRNA and protein levels. OPN expression is known to be associated
with chondrocyte and osteoblast differentiation and osteoclast activation.
Unexpectedly, FGF9 induced OPN was accompanied by inhibition of differentiation
and increased proliferation of the treated chondrocytes. Moreover, FGF9
stimulated OPN expression irrespective of the differentiation stage of the cells 
or culture conditions. In situ hybridization analysis of epiphyseal growth plates
from chicken or mice homozygous for the Achondroplasia, G369C/mFGFR3 mutation
demonstrated co-localization of OPN expression and osteoclast activity, as
evidenced by tartarate resistant acid phosphatase positive cells in the
osteochondral junction. We propose that FGF signaling directly activates OPN
expression independent of chondrocytes differentiation. This may enhance the
recruitment and activation of osteoclasts, and increase in cartilage resorption
and remodeling in the chondro-osseus border.

PMID: 16253490 [PubMed - indexed for MEDLINE]

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