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

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.