We investigated whether adenosine, a potent contributor to the regulation of pulmonary function, can modulate human lung mast cell (HLMC) fibrinolytic activity. Tissue plasminogen activator (tPA) activity and tPA transcript expression levels from a human mast cell line (HMC-1) and HLMC were monitored following adenosine application. Adenosine potentiated mast cell tPA activity and tPA gene expression in a dose-dependent manner. Adenosine effects were abolished in the presence of adenosine deaminase. HMC-1 cells predominantly expressed adenosine A2A and A2B receptor transcripts (A2A>>A2B>A3>>A1). In addition to A2A and A2B, A3 receptor transcripts were also abundantly found in HLMC (A2A>>A2B>>A3>>A1). Pharmacological and signalling studies suggest that the A2A receptor is the major subtype accounting for adenosine-induced mast cell tPA activity. Finally, the supernatant from HMC-1 cells treated with adenosine (24h) significantly increased fibrin clot lysis, while ZM241385, an A2A receptor antagonist, abolished this effect. This study provides the first data to demonstrate the potentiating effect of adenosine on mast cell tPA activity and fibrin clot lysis.
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