ADOA3R as a therapeutic target in experimental colitis: proof by validated high-density oligonucleotide microarray analysis

Inflamm Bowel Dis. 2006 Aug;12(8):766-89. doi: 10.1097/00054725-200608000-00014.

Abstract

Adenosine A3 receptors (ADOA3Rs) are emerging as novel purinergic targets for treatment of inflammatory diseases. Our goal was to assess the protective effect of the ADOA3R agonist N(6)-(3-iodobenzyl)-adenosine-5-N-methyluronamide (IB-MECA) on gene dysregulation and injury in a rat chronic model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)--induced colitis. It was necessary to develop and validate a microarray technique for testing the protective effects of purine-based drugs in experimental inflammatory bowel disease. High-density oligonucleotide microarray analysis of gene dysregulation was assessed in colons from normal, TNBS-treated (7 days), and oral IB-MECA-treated rats (1.5 mg/kg b.i.d.) using a rat RNU34 neural GeneChip of 724 genes and SYBR green polymerase chain reaction. Analysis included clinical evaluation, weight loss assessment, and electron paramagnetic resonance imaging/spin-trap monitoring of free radicals. Remarkable colitis-induced gene dysregulation occurs in the most exceptional cluster of 5.4% of the gene pool, revealing 2 modes of colitis-related dysregulation. Downregulation occurs in membrane transporter, mitogen-activated protein (MAP) kinase, and channel genes. Upregulation occurs in chemokine, cytokine/inflammatory, stress, growth factor, intracellular signaling, receptor, heat shock protein, retinoid metabolism, neural, remodeling, and redox-sensitive genes. Oral IB-MECA prevented dysregulation in 92% of these genes, histopathology, gut injury, and weight loss. IB-MECA or adenosine suppressed elevated free radicals in ex vivo inflamed gut. Oral IB-MECA blocked the colitis-induced upregulation (<or=20-fold) of Bzrp, P2X1R, P2X4R, P2X7R, P2Y2R, P2Y6R, and A2aR/A2bR but not A1R or A3R genes or downregulated P2X2R, P2Y1R, and P2Y4R. Real-time SYBR green polymerase chain reaction validated gene chip data for both induction of colitis and treatment with IB-MECA for >90% of genes tested (33 of 37 genes). We conclude that our validated high-density oligonucleotide microarray analysis is a powerful technique for molecular gene dysregulation studies to assess the beneficial effects of purine-based or other drugs in experimental colitis. ADOA3R is new potential therapeutic target for inflammatory bowel disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine / analogs & derivatives*
  • Adenosine / pharmacology
  • Adenosine / therapeutic use
  • Adenosine A3 Receptor Agonists*
  • Animals
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colitis / enzymology
  • Colitis / genetics
  • Disease Models, Animal
  • Free Radicals / metabolism
  • Gene Expression Regulation / drug effects*
  • Glutathione Peroxidase / metabolism
  • Oligonucleotide Array Sequence Analysis*
  • Polymerase Chain Reaction
  • Rats
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / metabolism
  • Trinitrobenzenesulfonic Acid

Substances

  • Adenosine A3 Receptor Agonists
  • Free Radicals
  • N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine
  • Trinitrobenzenesulfonic Acid
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Adenosine