Caveolin‑1 regulates oxidative stress‑induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Ding,Lei; Zeng,Qingmin; Wu,Jingping; Li,Defang; Wang,Houlei; Lu,Wei; Jiang,Zengxin; Xu,Guoxiong

doi:10.3892/mmr.2017.7789

Caveolin‑1 regulates oxidative stress‑induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Authors:
- Lei Ding
- Qingmin Zeng
- Jingping Wu
- Defang Li
- Houlei Wang
- Wei Lu
- Zengxin Jiang
- Guoxiong Xu
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Affiliations: Department of Orthopedic Surgery, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China, Central Laboratory, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China
Published online on: October 13, 2017 https://doi.org/10.3892/mmr.2017.7789
Pages: 9521-9527
Copyright: © Ding et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have indicated that cellular senescence is a critical underlying mechanism of intervertebral disc degeneration. However, the precise mechanism by which cellular senescence accelerates disc degeneration has not been fully elucidated. Caveolin‑1 has recently emerged as an important regulator of cellular senescence. Therefore, the aim of the present study was to investigate whether caveolin‑1 is involved in nucleus pulposus (NP) cellular senescence during oxidative stress. PCR was used to detect caveolin‑1 mRNA expression and protein expression was detected by western blotting. Caveolin‑1 expression at the mRNA and protein levels was markedly increased following treatment with tert‑butyl hydroperoxide, and an increase in premature senescence was observed, as determined by senescence‑associated β‑galactosidase staining and the decline of cellular proliferative ability. In addition, caveolin‑1 gene expression was successfully knocked down by lentivirus‑mediated RNA interference, which exerted a protective effect against the cellular senescence induced by oxidative stress. Notably, p53 and p21 protein expression, though not p16 protein expression, decreased with caveolin‑1 silencing. The results suggested that caveolin‑1 may be involved in NP cellular senescence during oxidative stress in vitro, mainly via the p53/p21 signaling pathway. Thus, caveolin‑1 may represent a novel therapeutic target for the prevention of intervertebral disc degeneration.

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