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Activation of the A3 adenosine receptor suppresses superoxide production and chemotaxis of mouse bone marrow neutrophils
Journal article   Peer reviewed

Activation of the A3 adenosine receptor suppresses superoxide production and chemotaxis of mouse bone marrow neutrophils

Dharini Van Der Hoeven, Tina C. Wan and John A. Auchampach
Molecular pharmacology, Vol.74(3), pp.685-696
09/2008
DOI: 10.1124/mol.108.048066
PMID: 18583455

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Abstract

Adenosine is formed in injured/ischemic tissues, where it suppresses the actions of essentially all cells of the immune system. Most of the anti-inflammatory actions of adenosine have been attributed to signaling through the Gs protein-coupled A2A adenosine receptor (AR). Here, we report that the A3AR is highly expressed in murine neutrophils isolated from bone marrow. Selective activation of the A3AR with (2S,3S,4R,5R)-3-amino-5-[6-(2,5-dichlorobenzylamino)purin-9-yl]-4-hydroxytetrahydrofuran-2-carboxylic acid methylamide (CP-532,903) potently inhibited mouse bone marrow neutrophil superoxide generation and chemotaxis induced by various activating agents. The selectivity of CP-532,903 was confirmed in assays using neutrophils obtained from A2AAR and A3AR gene “knockout” mice. In a model of thioglycollate-induced inflammation, treating mice with CP-532,903 inhibited recruitment of leukocytes into the peritoneum by specifically activating the A3AR. Collectively, our findings support the theory that the A3AR contributes to the anti-inflammatory actions of adenosine on neutrophils and provide a potential mechanistic explanation for the efficacy of A3AR agonists in animal models of inflammation (i.e., inhibition of neutrophil-mediated tissue injury).

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