• Yachuan Zhou, Xiaoqian Chen, Qinglu Tian, Jun Zhang, Mian Wan, Xin Zhou, Xin Xu, Xu Cao, Xuedong Zhou, and Liwei Zheng.
• State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases& Department of Cariology and Endodon-tics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
• Spine. 2022 Jun 15; 47 (12): 899-907.

Study DesignAnimal experiment: a mouse model of intervertebral disc (IVD) degeneration induced by deletion of apolipoprotein E (apoE).ObjectiveThe aim of this study was to investigate the role and mechanism of apoE on the process of IVD degeneration.Summary Of Background DataAbnormal lipid metabolism has been demonstrated to be closely related to IVD degeneration, a common chronic degenerative joint disease. ApoE, a component of apolipoproteins, plays a crucial role in lipid transportation and metabolic balance. But the relationship between apoE and IVD degeneration remains largely unknown.MethodsApoE knockout (KO) mouse was employed to investigate the progressive disc degeneration. The changes of vertebral bone and intervertebral disc space were measured by micro-computed tomography (micro-CT). The histo-morphological changes of cartilage endplate (CEP) and underlying signals were tested using immunohistochemistry and immunofluorescence staining.ResultsThe deletion of apoE gene accelerated the lumbar spine degeneration. Compared with WT mice, apoE KO mice showed reduced IVD space and increased vertebral bone mass. The progressive CEP degeneration was further found with cartilage degradation and endplate sclerosis in apoE KO mice. The deletion of apoE stimulated abnormal CEP bone remodeling and activation of adipokines signals.ConclusionThe deletion of apoE gene induced abnormal activation of adipokines signals, thus contribute to the CEP degeneration.Level Of EvidenceN/A.Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

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