c-Jun, krox-20, and integrin beta4 expression following chronic nerve compression injury

Limited work has been done to investigate the molecular mechanisms behind the process of demyelination and remyelination that occurs in response to chronic nerve compression (CNC) injury. In the present study, we investigated the expression of the transcription factors krox-20 and c-jun, positive and negative regulators of myelination, respectively. A decrease in krox-20 expression and an increase in c-jun expression in both its phosphorylated and non-phosphorylated states were observed. In addition, we investigated the role of integrins, specifically the beta4 subunit of the alpha6beta4 dimer, as a possible upstream signal transducer in the signaling cascade leading to demyelination. We detected a decrease in beta4 integrin expression at 2 and 4 weeks post-injury and a concomitant relocalization to the Schmidt-Lanterman Incisures, suggesting a role for the beta4 integrin in facilitating Schwann cell-extracellular matrix interaction. The observed changes in transcription factor and integrin expression are temporally correlated with the process of demyelination, and suggest further investigation to define their definitive role in regulating the myelin response to CNC injury.