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PKR and HMGB1 expression and function in rheumatoid arthritis

W J Wang1, S J Yin1, R Q Rong2

  • 1Spine Surgery, The People's Hospital of Shouguang, Shouguang, Shandong Province, China.

Genetics and Molecular Research : GMR
|January 20, 2016
PubMed

Insights

This study investigated the roles of double-stranded RNA-activated protein kinase (PKR) and high-mobility group box chromosomal protein 1 (HMGB1) in rheumatoid arthritis (RA). Inhibiting PKR reduced RA symptoms and HMGB1 levels in a rat model.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Rheumatoid arthritis (RA) pathogenesis involves inflammation.
  • The roles of double-stranded RNA-activated protein kinase (PKR) and high-mobility group box chromosomal protein 1 (HMGB1) in RA require further elucidation.

Purpose of the Study:

  • To investigate the involvement of PKR and HMGB1 in a rat model of RA.
  • To evaluate the therapeutic effect of a PKR-specific inhibitor on RA symptoms and associated molecular changes.

Main Methods:

  • An RA rat model was established using Freund's adjuvant injection.
  • Rats were treated with a PKR inhibitor (C16).
  • Limb swelling, plasma HMGB1 levels, and synovial PKR/HMGB1 expression (mRNA and protein) were assessed.

Main Results:

  • RA induction led to increased limb swelling, plasma HMGB1, and synovial PKR/HMGB1 levels.
  • PKR inhibition significantly reduced limb swelling and plasma HMGB1.
  • PKR inhibition also decreased elevated synovial PKR and HMGB1 expression.

Conclusions:

  • Elevated PKR and HMGB1 are implicated in RA development in this rat model.
  • Selective PKR inhibition demonstrates therapeutic potential for RA, possibly via HMGB1 pathway modulation.

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