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IDH2-Deficient Mice Develop Spinal Deformities With Agingopen access

Authors
Chae, U.Park, N.-R.Kim, E. S.Choi, J.-Y.Yim, M.Lee, H.-S.Lee, S.-R.Lee, S.Park, J.-W.Lee, D.-S.
Issue Date
Mar-2018
Publisher
ACAD SCIENCES CZECH REPUBLIC, INST PHYSIOLOGY
Keywords
Isocitrate dehydrogenase 2; Spinal deformity; Osteoclast; Osteoblast; Aging; Animal models
Citation
PHYSIOLOGICAL RESEARCH, v.67, no.3, pp 487 - 494
Pages
8
Journal Title
PHYSIOLOGICAL RESEARCH
Volume
67
Number
3
Start Page
487
End Page
494
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/4611
DOI
10.33549/physiolres.933711
ISSN
0862-8408
1802-9973
Abstract
Spinal deformities such as scoliosis and kyphosis are incurable, and can lead to decreased physical function, pain, and reduced quality of life. Despite much effort, no clear therapies for the treatment of these conditions have been found. Therefore, the development of an animal model for spinal deformity would be extremely valuable to our understanding of vertebral diseases. In this study, we demonstrate that mice deficient in the mitochondria! enzyme isocitrate dehydrogenase 2 (IDH2) develop spinal deformities with aging. We use morphological analysis as well as radiographic and micro-CT imaging of IDH2-deficient mice to characterize these deformities. Histological analysis showed increased abnormalities in IDH2-deficient mice compared to wild type mice. Taken together, the results suggest that IDH2 plays a critical role in maintaining the spinal structure by affecting the homeostatic balance between osteoclasts and osteoblasts. This indicates that IDH2 might be a potent target for the development of therapies for spinal deformities. Our findings also provide a novel animal model for vertebral disease research.
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