• Masaki Arioka, Fumi Takahashi-Yanaga, Masanori Sasaki, Tatsuya Yoshihara, Sachio Morimoto, Akihiko Takashima, Yoshihide Mori, and Toshiyuki Sasaguri.
• Department of Clinical Pharmacology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan; Department of Oral and Maxillofacial Surgery, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
• Biochem. Biophys. Res. Commun. 2013 Nov 1; 440 (4): 677-82.

AbstractGlycogen synthase kinase (GSK)-3β plays an important role in osteoblastogenesis by regulating the Wnt/β-catenin signaling pathway. Therefore, we investigated whether GSK-3β deficiency affects bone development and regeneration using mice heterozygously deficient for GSK-3β (GSK-3β(+/-)). The amounts of β-catenin, c-Myc, cyclin D1, and runt-related transcription factor-2 (Runx2) in the bone marrow cells of GSK-3β(+/-) mice were significantly increased compared with those of wild-type mice, indicating that Wnt/β-catenin signals were enhanced in GSK-3β(+/-) mice. Microcomputed tomography of the distal femoral metaphyses demonstrated that the volumes of both the cortical and trabecular bones were increased in GSK-3β(+/-) mice compared with those in wild-type mice. Subsequently, to investigate the effect of GSK-3β deficiency on bone regeneration, we established a partial bone defect in the femur and observed new bone at 14 days after surgery. The volume and mineral density of the new bone were significantly higher in GSK-3β(+/-) mice than those in wild-type mice. These results suggest that bone formation and regeneration in vivo are accelerated by inhibition of GSK-3β, probably through activation of the Wnt/β-catenin signaling pathway.Copyright © 2013 Elsevier Inc. All rights reserved.

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