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Different roles of peripheral mitogen-activated protein kinases in carrageenan-induced arthritic pain and arthritis

Hongxiu Han1, Kyu-Sang Lee, Weifang Rong

  • 1Department of Pathology, No. 3 People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.

Anesthesia and Analgesia
|July 24, 2012
PubMed
Abstract

Insights

Peripheral extracellular signal-regulated protein kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) pathways play distinct roles in arthritic pain and knee joint inflammation, influencing pain behaviors and inflammatory responses differently.

Area of Science:

  • Pain research
  • Molecular biology
  • Inflammation studies

Background:

  • Extracellular signal-regulated protein kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) are implicated in pain hypersensitivity.
  • Direct evidence for their role in peripheral arthritic pain and arthritis development is limited.

Purpose of the Study:

  • To investigate the involvement of peripheral ERK, p38, and JNK in the induction and maintenance of arthritic pain and inflammation in a rat model.
  • To evaluate the effects of selective inhibitors of these kinases on pain-related behaviors and inflammatory responses.

Main Methods:

  • Intra-articular administration of selective inhibitors for p38 (SB203580), JNK (SP600125), and MEK (PD98059) to indirectly inhibit ERK.
  • Assessment of weight-bearing reduction, neutrophil infiltration, and knee joint diameter.
  • Examination of phosphorylated ERK, p38, and JNK levels in synovial tissue via Western blot.

Main Results:

  • Pretreatment with PD98059, SB203580, and SP600125 prevented weight load reduction, with varying time courses.
  • Therapeutic administration of PD98059 and SB203580 partially reversed weight load reduction.
  • SB203580 and SP600125 inhibited neutrophil infiltration, while PD98059 did not.
  • Distinct temporal expression patterns of phosphorylated ERK, p38, and JNK were observed in the synovium.

Conclusions:

  • Peripheral ERK, p38, and JNK signaling pathways exhibit differential involvement in arthritic pain and knee joint inflammation.
  • These findings highlight distinct roles for these kinases in the pathogenesis of arthritis.

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