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GluN2B/CaMKII mediates CFA-induced hyperalgesia via HDAC4-modified spinal COX2 transcription

Cheng-Yuan Lai1, Ming-Chun Hsieh2, Yu-Cheng Ho3

  • 1Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, Taichung, Taiwan; Department of Medicine, Mackay Medical College, New Taipei, Taiwan.

Neuropharmacology
|April 4, 2018
PubMed

Insights

Inflammatory pain involves epigenetic changes mediated by histone deacetylase 4 (HDAC4). This study shows HDAC4

Area of Science:

  • Neuroscience
  • Epigenetics
  • Pain Research

Background:

  • Histone deacetylase 4 (HDAC4) is involved in epigenetic regulation.
  • Its role in inflammatory pain and neural plasticity is not well understood.

Purpose of the Study:

  • To investigate the role of HDAC4-dependent epigenetic mechanisms in the development of inflammatory pain.
  • To explore the upstream signaling pathways regulating HDAC4 activity in pain.

Main Methods:

  • Inflammatory pain was induced in rats using Complete Freund's Adjuvant (CFA).
  • HDAC4 phosphorylation and localization in dorsal horn neurons were analyzed.
  • COX2 expression and its relation to HDAC4 and upstream signaling were examined.

Main Results:

  • CFA injection induced hyperalgesia, HDAC4 phosphorylation, and cytoplasmic redistribution in dorsal horn neurons.
  • Cytoplasmic HDAC4 was uncoupled from the COX2 promoter, increasing spinal COX2 expression.
  • The GluN2B-NMDAR/CaMKII pathway was identified as an upstream regulator of HDAC4 activity in inflammatory pain.

Conclusions:

  • Spinal HDAC4-dependent epigenetic mechanisms are involved in the development and maintenance of inflammatory pain.
  • Targeting HDAC4 offers a potential new strategy for managing inflammatory pain.
Keywords:
COX2CaMKIIGluN2BHDAC4Inflammatory painNMDA

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