The anti-inflammatory target A3 adenosine receptor is over-expressed in rheumatoid arthritis, psoriasis and Crohn's disease

A. Ochaion, S. Bar-Yehuda, S. Cohen, F. Barer, R. Patoka, H. Amital, T. Reitblat, A. Reitblat, J. Ophir, I. Konfino, Y. Chowers, S. Ben-Horin, P. Fishman*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

98 Scopus citations

Abstract

The Gi protein associated A3 adenosine receptor (A3AR) was recently defined as a novel anti-inflammatory target. The aim of this study was to look at A3AR expression levels in peripheral blood mononuclear cells (PBMCs) of patients with autoimmune inflammatory diseases and to explore transcription factors involved receptor expression. Over-expression of A3AR was found in PBMCs derived from patients with rheumatoid arthritis (RA), psoriasis and Crohn's disease compared with PBMCs from healthy subjects. Bioinformatics analysis demonstrated the presence of DNA binding sites for nuclear factor-κB (NF-κB) and cyclic AMP-responsive element binding protein (CREB) in the A3AR gene promoter. Up-regulation of NF-κB and CREB was found in the PBMCs from patients with RA, psoriasis and Crohn's disease. The PI3K-PKB/Akt signaling pathway, known to regulate both the NF-κB and CREB, was also up-regulated in the patients' PBMCs. Taken together, NF-κB and CREB are involved with the over-expression of A3AR in patients with autoimmune inflammatory diseases. The receptor may be considered as a specific target to combat inflammation.

Original languageEnglish
Pages (from-to)115-122
Number of pages8
JournalCellular Immunology
Volume258
Issue number2
DOIs
StatePublished - 2009

Keywords

  • A adenosine receptor
  • ADORA3
  • CREB
  • Crohn's disease
  • Inflammation
  • NF-κB
  • PI3K-PKB/Akt
  • Psoriasis
  • Rheumatoid arthritis

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