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BioMed Research International
Volume 2017 (2017), Article ID 8215805, 7 pages
Research Article

Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice

1Academy of Orthopedics of Guangdong Province, Department of Orthopedic Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China
2Department of Anesthesia, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
3Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou 510060, China
4Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou 510515, China
5Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China

Correspondence should be addressed to Dadi Jin; moc.361@pohtroyn, Xiaochun Bai; nc.ude.ums@51cxiab, and Rongping Zhou; moc.621@1428168gnor

Received 21 December 2016; Accepted 13 March 2017; Published 24 April 2017

Academic Editor: Ruijin Huang

Copyright © 2017 Cheng Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Congenital spinal deformity is the most severe clinical orthopedic issue worldwide. Among all the pathological processes of congenital spinal deformity, the imbalance of endochondral ossification is considered to be the most important developmental cause of spinal dysplasia. We established chondrocyte-specific TSC-1 knockout (KO) mice to overactivate the energy metabolic component, mammalian target of rapamycin complex 1 (mTORC1), and measured the spinal development by general, imaging, histological, and Western-blot assessments. In addition to skeletal dysplasia, the KO mice displayed severe congenital spinal deformity and significant intervertebral disc changes. This study suggests that, in the process of endochondral ossification, excessive activation of mTORC1 signaling in chondrocytes induces obvious spinal deformity, and the chondrocytes may be the cell type responsible for congenital spinal deformity.