Protein kinase C theta (Prkcq) affects nerve degeneration and regeneration through the c-fos and c-jun pathways in injured rat sciatic nerves

Background: Previous finding using DNA microarray and bioinformatics analysis, we have reported some key factors which regulated gene expression and signaling pathways in injured sciatic nerve during Wallerian Degeneration (WD). This research is focused on protein kinase C theta (Prkcq) participates in the regulation of the WD process. Methods: In this study, we explored the molecular mechanism by which Prkcq in Schwann cells (SCs) affects nerve degeneration and regeneration in vivo and in vitro after rat sciatic nerve injury. Results: Study of the cross-sectional model showed that Prkcq expression decreased significantly during sciatic nerve repair. Functional analysis showed that upregulation and downregulation of Prkcq could affect the proliferation, migration and apoptosis of Schwann cells and lead to the expression of related factors through the activation of the beta-catenin, c-fos, and p-c-jun/c-jun pathways. Conclusion: The study provides insights into the role of Prkcq in early WD during peripheral nerve degeneration and/or regeneration.

Automated summary

This study investigates the role of Prkcq in regulating nerve degeneration and regeneration, with findings showing that modulation of Prkcq expression can affect the function of Schwann cells and related signaling pathways. The results provide insights into the molecular mechanisms involved in Prkcq-mediated processes during peripheral nerve repair.