Background: The cells of the intervertebral disc must synthesise and maintain their surrounding matrix for it to function normally, providing all its physiological and mechanical properties. However, disc cells survive in an environment that most cells would not tolerate, ie with a low pH and relatively little oxygen. Cells which experience such potentially damaging conditions, including excessive heat, elicit a stress response and synthesise a range of proteins, called heat shock proteins (Hsps); these facilitate repair and survival or removal of damaged cells.

Methods and Results: We have studied Hsp production by disc cells, both in vitro and in vivo. We measured Hsps produced by bovine skin and disc cells grown in monolayer and heated up to 45°C and also immunostained human surgical discs for stress proteins, Hsp27 and Hsp72.

Disc cells responded differently to dermal fibroblasts; when freshly isolated they had a reduced or attenuated stress response and produced much less Hsp 70 than freshly isolated skin cells. After culturing in monolayer (by passage 2) all cells produced more Hsps. Human surgical discs produced varying amounts of Hsp, with most being produced by cells in herniated discs, particularly those within clusters of cells.

Conclusion: Our results suggest that intervertebral disc cells in vivo normally have a reduced stress response. Hsp production is considered to protect against damage, suggesting that the reduced response may contribute to disc degeneration and back pain. The prosurvival stress response of disc cells could provide a novel therapeutic target in patients with degenerative disc disease.

Conflict of Interest: None

Source of Funding: Wolfson Charitable Trust