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SIRPα1-SHP2 Interaction Regulates Complete Freund Adjuvant-Induced Inflammatory Pain via Src-Dependent GluN2B

Cheng-Yuan Lai1, Tzer-Bin Lin, Ming-Chun Hsieh

  • 1From the Department of Medicine, Mackay Medical College, New Taipei, Taiwan; Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan; Department of Biotechnology, Asia University, Taichung, Taiwan; Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan; Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Physiology, School of Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; and Department of Obstetrics and Gynecology, Chung-Shan Medical University Hospital, Chung-Shan Medical University, Taichung, Taiwan.

Anesthesia and Analgesia
|January 1, 2016
PubMed
Abstract

Insights

The signal regulatory protein alpha1 (SIRPα1)-activated spinal SHP2/Src cascade and GluN2B phosphorylation are key mediators of inflammatory pain. Targeting this SIRPα1-SHP2 pathway offers a potential strategy for pain relief.

Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Understanding pain mechanisms is crucial for developing effective treatments.
  • The role of the SIRPα1-activated spinal SHP2/Src cascade and GluN2B phosphorylation in inflammatory pain remains unclear.

Purpose of the Study:

  • To investigate the involvement of the SIRPα1-activated spinal SHP2/Src cascade and downstream GluN2B phosphorylation in inflammatory pain.
  • To explore potential therapeutic targets for inflammatory pain management.

Main Methods:

  • Complete Freund's adjuvant (CFA) induced inflammatory pain model in rodents.
  • Assessment of paw withdrawal latency using the Hargreaves test.
  • Western blotting and immunoprecipitation analysis of dorsal horn (L4-L5) samples.

Main Results:

  • CFA injection induced hyperalgesia and increased expression of SIRPα1, pSHP2, pSrc, and pGluN2B.
  • SIRPα1-neutralizing antibody and SHP2 antagonist (NSC 8787) dose-dependently attenuated hyperalgesia and related signaling.
  • Src inhibitor (PP2) reduced hyperalgesia but did not affect SHP2 phosphorylation or associated signaling.

Conclusions:

  • CFA-induced spinal SIRPα1 expression triggers SHP2 and Src phosphorylation, leading to pSrc-GluN2B interaction and activation, contributing to inflammatory pain.
  • Targeting spinal SIRPα1-SHP2 coupling presents a promising strategy for inflammatory pain relief.

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