Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice
| Autor: | Rong-Ping Zhou, Xiaochun Bai, Daozhang Cai, Pinglin Lai, Bin Huang, Dadi Jin, Jiajun Tang, Yuhui Chen, Cheng Yang, He Cao, Bo Yan, Zhen Li, Shicai Fan, Keming Chen |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cell type Pathology medicine.medical_specialty Article Subject lcsh:Medicine Mechanistic Target of Rapamycin Complex 1 General Biochemistry Genetics and Molecular Biology Chondrocyte Bone and Bones Tuberous Sclerosis Complex 1 Protein 03 medical and health sciences Mice Chondrocytes Osteogenesis Medicine Animals Pathological Endochondral ossification Mice Knockout General Immunology and Microbiology business.industry Tumor Suppressor Proteins lcsh:R Spinal dysplasia Intervertebral disc Cell Differentiation General Medicine medicine.disease 030104 developmental biology medicine.anatomical_structure Dysplasia Orthopedic surgery Spinal Diseases business Chondrogenesis Research Article Signal Transduction |
| Zdroj: | BioMed Research International BioMed Research International, Vol 2017 (2017) |
| ISSN: | 2314-6141 2314-6133 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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