
Proteomic and Phosphoproteomic Changes of MAPK-Related Inflammatory Response in an Animal Model of Neuropathic Pain by Differential Target Multiplexed SCS and Low-Rate SCS
Author(s) -
David L. Cedeño,
Dana M. Tilley,
Francesco Vetri,
David C. Platt,
Ricardo Vallejo
Publication year - 2022
Publication title -
journal of pain research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 49
ISSN - 1178-7090
DOI - 10.2147/jpr.s348738
Subject(s) - medicine , neuropathic pain , kinase , neuroinflammation , signal transduction , phosphorylation , sni , phosphoproteomics , proteomics , microbiology and biotechnology , pharmacology , inflammation , immunology , protein kinase a , biology , protein phosphorylation , biochemistry , gene , hydrolysis , acid hydrolysis
Neuropathic pain initiates an interplay of pathways, involving MAP kinases and NFκB-signaling, leading to expression of immune response factors and activation and inactivation of proteins via phosphorylation. Neuropathic pain models demonstrated that spinal cord stimulation (SCS) may provide analgesia by modulating gene and protein expression in neuroinflammatory processes. A differential target multiplexed programming (DTMP) approach was more effective than conventional SCS treatments at modulating these. This work investigated the effect of DTMP and low rate SCS (LR-SCS) on proteins associated with MAP kinases and NFκB-signaling relevant to neuroinflammation.