PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia.

Postherpetic neuralgia (PHN) is a chronic pain condition that develops in the area of a previous herpes zoster (shingles) infection. Protein tyrosine phosphatase receptor type K (PTPRK) encodes a receptor-type protein tyrosine phosphatase involved in regulating cell signaling, growth, and neural development. p38 MAPK signaling pathway regulates cellular responses to stress, inflammation, and cytokines, influencing processes like cell differentiation, apoptosis, and immune response. This study aimed to discover the role of PTPRK in PHN and the underlying mechanism. Bioinformatics analysis was used to screen for differentially expressed genes and enrichment pathways of these genes in PHN and control groups. Resiniferatoxin (RTX) was used to induce rat PHN model. Mechanical allodynia and thermal hypoalgesia were assessed by measuring the paw withdrawal threshold and latency. The levels of inflammatory cytokines were detected by ELISA and RT-qPCR. Western blot was performed to analyze the protein levels of DUSP1/p38 MAPK signaling pathway. Results showed that PTPRK expression was increased in RTX-induced rat PHN model. Besides, PTPRK promoted mechanical allodynia, thermal hypoalgesia, and inflammation in RTX-induced rat PHN model via activating DUSP1/p38 MAPK signaling pathway in rat dorsal root ganglia (DRG) tissues. In addition, PTPRK overexpression promoted inflammation by activating DUSP1/p38 MAPK signaling pathway in rat DRG cells. In conclusion, PTPRK promoted RTX-induced PHN via activating DUSP1/p38 MAPK signaling pathway in DRG, which might provide a reference for the treatment of PHN.