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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
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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
Summary
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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