| First Author | Arioka M | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 440 |
| Issue | 4 | Pages | 677-82 |
| PubMed ID | 24099767 | Mgi Jnum | J:211406 |
| Mgi Id | MGI:5575418 | Doi | 10.1016/j.bbrc.2013.09.126 |
| Citation | Arioka M, et al. (2013) Acceleration of bone development and regeneration through the Wnt/beta-catenin signaling pathway in mice heterozygously deficient for GSK-3beta. Biochem Biophys Res Commun 440(4):677-82 |
| abstractText | Glycogen synthase kinase (GSK)-3beta plays an important role in osteoblastogenesis by regulating the Wnt/beta-catenin signaling pathway. Therefore, we investigated whether GSK-3beta deficiency affects bone development and regeneration using mice heterozygously deficient for GSK-3beta (GSK-3beta(+/-)). The amounts of beta-catenin, c-Myc, cyclin D1, and runt-related transcription factor-2 (Runx2) in the bone marrow cells of GSK-3beta(+/-) mice were significantly increased compared with those of wild-type mice, indicating that Wnt/beta-catenin signals were enhanced in GSK-3beta(+/-) mice. Microcomputed tomography of the distal femoral metaphyses demonstrated that the volumes of both the cortical and trabecular bones were increased in GSK-3beta(+/-) mice compared with those in wild-type mice. Subsequently, to investigate the effect of GSK-3beta 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-3beta(+/-) mice than those in wild-type mice. These results suggest that bone formation and regeneration in vivo are accelerated by inhibition of GSK-3beta, probably through activation of the Wnt/beta-catenin signaling pathway. |
