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

BioMed Research International
Cheng YangRongping Zhou

Abstract

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.

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Citations

Feb 13, 2019·Annals of the Rheumatic Diseases·Wenxue TongKingston King-Lun Mak
Jan 26, 2021·Frontiers in Cell and Developmental Biology·Martina La SpinaJosé A Martina

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Methods Mentioned

BETA
X-ray
genotyping

Software Mentioned

SPSS
MED

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