TY - JOUR
T1 - Functional requirement of CCN2 for intramembranous bone formation in embryonic mice
AU - Kawaki, Harumi
AU - Kubota, Satoshi
AU - Suzuki, Akiko
AU - Yamada, Tomohiro
AU - Matsumura, Tatsushi
AU - Mandai, Toshiko
AU - Yao, Mayumi
AU - Maeda, Takeyasu
AU - Lyons, Karen M.
AU - Takigawa, Masaharu
N1 - Funding Information:
The authors thank Drs. Takako Hattori, Takashi Nishida, for their helpful suggestions; Ms. Tomoko Yamamoto for technical assistance and Ms. Yuki Nonami for valuable secretarial assistance. This work was supported by Grants-in-Aid for Scientific Research (S) (to M.T.), (C) (to S.K.) and Exploratory Research (to M.T.) from the Ministry of Education, Culture, Sports, Science. H.K. is a recipient of the Iwadare Scholarship from the Iwadare Educational Association for Dental Graduate Students.
PY - 2008/2/8
Y1 - 2008/2/8
N2 - 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.
AB - 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.
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U2 - 10.1016/j.bbrc.2007.11.155
DO - 10.1016/j.bbrc.2007.11.155
M3 - Article
C2 - 18067859
AN - SCOPUS:37449000249
SN - 0006-291X
VL - 366
SP - 450
EP - 456
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -