Caveolin-1 expression and stress-induced premature senescencein human intervertebral disc degeneration

Sarah Kathleen Heathfield, Christine Lyn Le Maitre, Judith Alison Hoyland

    Research output: Contribution to journalArticlepeer-review


    Chronic and debilitating low back pain is a common condition and a huge economic burden. Many cases are attributed to age-related degeneration of the intervertebral disc (IVD); however, age-related degeneration appears to occur at an accelerated rate in some individuals. We have previously demonstrated biomarkers of cellular senescence within the human IVD and suggested a role for senescence in IVD degeneration. Senescence occurs with ageing but can also occur prematurely in response to stress. We hypothesised that stress-induced premature senescence (SIPS) occurs within the IVD and here we have investigated the expression and production of caveolin-1, a protein that has been shown previously to be upregulated in SIPS.

    Caveolin-1 gene expression in human nucleus pulposus (NP) cells was assessed by conventional and quantitative real-time polymerase chain reaction (PCR), and caveolin-1 protein expression was examined within human IVDs using immunohistochemistry. The correlation between caveolin-1 and p16INK4a (biomarker of cellular senescence) gene expression was investigated using quantitative real-time PCR

    Caveolin-1 gene expression and protein expression were demonstrated within the human IVD for the first time. NP cells from degenerate discs exhibited elevated levels of caveolin-1 which did not relate to increasing chronological age. A negative correlation was observed between gene expression for caveolin-1 and donor age, and no correlation was found between caveolin-1 protein expression and age. A positive correlation was identified between gene expression of caveolin-1 and p16INK4a.

    Our findings are consistent with a role for caveolin-1 in degenerative rather than age-induced changes in the NP. Its expression in IVD tissue and its association with the senescent phenotype suggest that caveolin-1 and SIPS may play a prominent role in the pathogenesis of IVD degeneration.
    Original languageEnglish
    Article numberR87
    JournalArthritis Research and Therapy
    Issue number4
    Publication statusPublished - 5 Aug 2008


    • Adult
    • Aged
    • metabolism: Aging, Premature
    • metabolism: Biological Markers
    • metabolism: Caveolin 1
    • metabolism: Cyclin-Dependent Kinase Inhibitor p16
    • Humans
    • metabolism: Intervertebral Disk
    • Middle Aged
    • etiology: Spinal Diseases
    • physiology: Stress, Physiological


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