Abstract
Introduction
Cytokeratin 8 (CK8) is a member of the cytokeratins family with multiple functions on the basis of its unique structural hallmark. The aberrant expression of CK8 and its phosphorylation are pertinent with various diseases. We have previously shown that CK8 exists in normal human nucleus pulposus (NP) cells and decreases as the intervertebral disc degenerates. However, the underlying molecular regulatory machinery of CK8 in intervertebral disc degeneration (IDD) has not been clarified.
Materials and Methods
NP samples were collected from patients with idiopathic scoliosis as control and IDD as degenerate groups. Phosphorylation of CK8 was detected. Moreover, NP cells were cultured under different compressive load schemes for diverse time duration.
Results
We found that CK8 expression decreased in IDD with an increased phosphorylation in degenerate NP cells. Moreover, compressive loads resulted in phosphorylation and disassembly of CK8 in a time-dependent and degree-dependent manner in vitro. The activation of protein kinase C (PKC) was a significant molecular factor contributing to this phenomenon.
Conclusion
This study is the first addressing the molecular mechanisms of CK8 downregulation in NP cells. Importantly, our findings provide clues regarding a molecular link between compressive loads and CK8 alterations, which shed a novel light on the etiology of IDD.
None declared