Figure 7.

Schematic illustration summarizing static compression-induced notochordal cell disappearance and apoptotic cell death in the intervertebral disc. The number of disc nucleus pulposus (NP) and annulus fibrosus (AF) cells decreases with compression; particularly, the decrease is notable in larger, vacuolated cells with a notochordal phenotype, cytokeratin-8+ galectin-3+. Subsequently, the proportion of apoptotic terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells and cleaved caspase-3-positive cells increases throughout. This apoptosis induction is mediated transiently through the death receptor pathway, as determined by immunopositivity for cleaved caspase-8, and persistently through the p53-dependent mitochondrial pathway, as identified by immunopositivity for cleaved caspase-9 and p53-regulated apoptosis-inducing protein 1 (p53AIP1). The percentage of cells expressing antiapoptotic proteins, B-cell lymphoma 2 (Bcl-2), and silent mating-type information regulation 2 homolog 1 (SIRT1), decreases consistently. The increased proapoptotic and decreased antiapoptotic proteins are an indication of static compression-induced disc cell death and degeneration.

Yurube et al. Arthritis Research & Therapy 2014 16:R31   doi:10.1186/ar4460
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