Protective effect of p53 on the viability of intervertebral disc nucleus pulposus cells under low glucose condition

- Low glucose induced p53 leakage from nuclei to cytoplasm in nucleus pulposus cells.
- P53 inhibited autophgy induced by low glucose in nucleus pulposus cells.
- P53 neutralized type II collagen decrease induced by low glucose in nucleus pulposus cells.
- P53 inhibited pentose phosphate pathway in nucleus pulposus cells.

P53 is a famous cancer suppressor and plays key roles in metabolism. Intervertebral disc (IVD) is the largest avascular cartilaginous structure in humans and its degeneration is a common cause of spine diseases initiated from damaged nucleus pulposus (NP) cells. The potential cause of disc degeneration has been attributed to aging, genetic factors, mechanical factors and nutrition. In this study, we found that p53 decreased and leaked to the cytoplasm in NP cells as the glucose level decreases, in contrast to cancer cells in which p53 increases and concentrates to the nuclei. Comparing with in p53 knockdown NP cells, relative high p53 expression in normal control NP cells inhibited autophagy and the pentose phosphate pathway. Furthermore, the expression of Sox 9 and type II collagen were higher in p53 normal control than p53 knockdown NP cells. Based on these results, we believe that relative high p53 facilitates NP cell viability and integrity.