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FGF18 accelerates osteoblast differentiation by upregulating B mp2 expression
Author(s) -
Nagayama Tomoko,
Okuhara Shigeru,
Ota Masato S.,
Tachikawa Noriko,
Kasugai Shohei,
Iseki Sachiko
Publication year - 2013
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/cga.12012
Subject(s) - downregulation and upregulation , osteoblast , mesenchyme , fibroblast growth factor , bone morphogenetic protein 2 , microbiology and biotechnology , coronal suture , parietal bone , endocrinology , fibroblast growth factor receptor 1 , chemistry , biology , medicine , receptor , anatomy , coronal plane , mesenchymal stem cell , biochemistry , skull , in vitro , gene
Fibroblast growth factor ( FGF ) signaling is involved in skeletal development. Among total 22 FGFs , it is suggested that FGF18 functions in promotion of osteoblast differentiation. In order to elucidate the mechanism of FGF18 ‐dependent acceleration of osteogenesis, we implanted rhFGF18 soaked beads over mouse fetal coronal sutures using ex‐utero surgery. The coronal suture area comprises the peripheries of the developing frontal and parietal bones, separated by the sutural mesenchyme. rhFGF18 accelerated osteogenesis by promoting connection of the frontal and parietal bone domains, resulting in elimination of the sutural mesenchyme. Expression of F gf receptors , F gfr1 , ‐ 2 and ‐ 3 involved in skeletal development, was maintained or upregulated in the developing bone domains, consistent with enhanced osteogenesis. B one morphogenetic protein ( B mp ) 2 was specifically upregulated in the skeletogenic layer and the application of B mp antagonist, rmNoggin, inhibited rhFGF18 ‐dependent upregulation of osteoblast markers. These results suggest that FGF18 accelerates osteogenesis by upregulation of B mp2 as well as maintenance or upregulation of F gfr1 , ‐ 2 and ‐ 3 expression in osteoblasts.