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ISSN 1449-2288 |
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International Journal of Medical Sciences Journal of Bone and Joint Infection (JBJI) ![]() ![]() |
Int J Biol Sci 2017; 13(12):1540-1546. doi:10.7150/ijbs.23000 Research Paper Specific Deletion of β-Catenin in Col2-Expressing Cells Leads to Defects in Epiphyseal Bone 1. Department of Pharmacy, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai 200011, China The role of canonical Wnt/β-catenin signaling in postnatal bone growth has not been fully defined. In the present studies, we generated β-catenin conditional knockout (KO) mice and deleted β-catenin in Col2-expressing chondrocytes and mesenchymal progenitor cells. Findings from analyzing the β-cateninCol2CreER KO mice revealed severe bone destruction and bone loss phenotype in epiphyseal bone, probably due to the increase in osteoclast formation and the accumulation of adipocytes in this area. In addition, we also found bone destruction and bone loss phenotype in vertebral bone in β-cateninCol2CreER KO mice. These findings indicate that β-catenin signaling plays a critical role in postnatal bone remodeling. Our study provides new insights into the regulation of epiphyseal bone homeostasis at postnatal stage. Keywords: Epiphysis, Wnt/β-Catenin Signaling, Postnatal Bone Growth, Osteoarthritis This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
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to cite this article:
Wang T, Li J, Zhou GQ, Ma P, Zhao Y, Wang B, Chen D. Specific Deletion of β-Catenin in Col2-Expressing Cells Leads to Defects in Epiphyseal Bone. Int J Biol Sci 2017; 13(12):1540-1546. doi:10.7150/ijbs.23000. Available from http://www.ijbs.com/v13p1540.htm |