Full text of this item is not currently available on the LRA. \ud The final published version is available at http://www.jimmunol.org/content/186/2/1209, Doi: 10.4049/jimmunol.1001563.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.\ud HMC-1 cells and HLMC predominantly expressed adenosine A2A and A2B receptor transcripts (A2B ≈ A2A > A3 >> A1).\ud Pharmacological and signaling 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 and HLMC treated with adenosine (for 24 h) significantly increased fibrin clot lysis, whereas ZM241385, an A2A receptor antagonist, abolished this effect. To our knowledge, 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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