Functional requirement of CCN2 for intramembranous bone formation in embryonic mice

CCN2 is best known as a promoter of chondrocyte differentiation among the CCN family members, and Ccn2 null mutant mice display skeletal dysmorphisms. However, little is known concerning the roles of CCN2 during bone formation. We herein present a comparative analysis of wild-type and Ccn2 null mice...

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Published in:Biochemical and biophysical research communications 2008-02, Vol.366 (2), p.450-456
Main Authors: Kawaki, Harumi, Kubota, Satoshi, Suzuki, Akiko, Yamada, Tomohiro, Matsumura, Tatsushi, Mandai, Toshiko, Yao, Mayumi, Maeda, Takeyasu, Lyons, Karen M., Takigawa, Masaharu
Format: Article
Language:English
Subjects:
Animals
CCN family
Cells, Cultured
Connective Tissue Growth Factor
Differentiation
Immediate-Early Proteins - metabolism
Intercellular Signaling Peptides and Proteins - metabolism
Intramembranous bone formation
Mice - embryology
Mice - metabolism
Null mutant
Osteoblast
Osteoblasts - physiology
Osteogenesis - physiology
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Summary:CCN2 is best known as a promoter of chondrocyte differentiation among the CCN family members, and Ccn2 null mutant mice display skeletal dysmorphisms. However, little is known concerning the roles of CCN2 during bone formation. We herein present a comparative analysis of wild-type and Ccn2 null mice to investigate the roles of CCN2 in bone development. Multiple histochemical methods were employed to analyze the effects of CCN2 deletion in vivo, and effects of CCN2 on the osteogenic response were evaluated with the isolated and cultured osteoblasts. As a result, we found a drastic reduction of the osteoblastic phenotype in Ccn2 null mutants. Importantly, addition of exogenous CCN2 promoted every step of osteoblast differentiation and rescued the attenuated activities of the Ccn2 null osteoblasts. These results suggest that CCN2 is required not only for the regulation of cartilage and subsequent events, but also for the normal intramembranous bone development.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.11.155