Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/124182
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Type: Journal article
Title: p16 deficiency attenuates intervertebral disc degeneration by adjusting oxidative stress and nucleus pulposus cell cycle
Author: Che, H.
Li, J.
Li, Y.
Ma, C.
Liu, H.
Qin, J.
Dong, J.
Zhang, Z.
Xian, C.J.
Miao, D.
Wang, L.
Ren, Y.
Citation: eLife, 2020; 9:1-23
Publisher: eLife
Issue Date: 2020
ISSN: 2050-084X
2050-084X
Statement of
Responsibility: 
Hui Che, Jie Li, You Li, Cheng Ma, Huan Liu, Jingyi Qin ... Cory J Xian ... et al.
Abstract: The cell cycle regulator p16 is known as a biomarker and an effector of aging. However, its function in intervertebral disc degeneration (IVDD) is unclear. In this study, p16 expression levels were found to be positively correlated with the severity of human IVDD. In a mouse tail suspension (TS)-induced IVDD model, lumbar intervertebral disc height index and matrix protein expression levels were reduced significantly were largely rescued by p16 deletion. In TS mouse discs, reactive oxygen species levels, proportions of senescent cells, and the senescence-associated secretory phenotype (SASP) were all increased, cell cycling was delayed, and expression was downregulated for Sirt1, superoxide dismutase 1/2, cyclin-dependent kinases 4/6, phosphorylated retinoblastoma protein, and transcription factor E2F1/2. However, these effects were rescued by p16 deletion. Our results demonstrate that p16 plays an important role in IVDD pathogenesis and that its deletion attenuates IVDD by promoting cell cycle and inhibiting SASP, cell senescence, and oxidative stress.
Keywords: cell cycle
cell proliferation
human
human biology
immunology
inflammation
intervertebral disc degeneration
medicine
mouse
oxidative stress
p16
Rights: © Copyright Che et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
DOI: 10.7554/eLife.52570
Grant ID: http://purl.org/au-research/grants/nhmrc/1158402
http://purl.org/au-research/grants/nhmrc/1127396
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