GSE113199
HO1 activates autophagy to protect intervertebral disc degeneration
Intervertebral disc degeneration (IDD) is majorly resulted from disordered extracellular matrix (ECM) metabolism, including decreased anabolism and increased catabolism activities in the nucleus pulposus (NP) cells of discs. Pro-inflammatory cytokines such as interleukin-1ß (IL-1ß) are considered to be potent mediators of ECM loss. We reported previously that hemeoxygenase-1 (HO-1) inducer cobalt protoporphyrin IX (CoPP) could attenuate the ECM breakdown which induced by IL-1ß, however, the underlying mechanism remains elusive. Here we found that autophagy family genes were involved in the HO-1 mediated anti-inflammatory processes in human NP cells by using high throughput RNA-Seq technique. These findings suggest that autophagy might play a role in inflammation related ECM metabolism disorder, thus offering a direction of our in-depth study and providing a framework for the searching of potential therapeutic targets in the treatment of IDD Overall design: Examination of the gene expression profile of human nucleus pulposus cells treated with CoPP or/and Interlukin-1ß