Figure 6
Figure 6. Adenosine kinase (AK) in modulating intracellular adenosine concentration and adenosine uptake. (A) Confluent HMEC-1s were exposed to normoxia or hypoxia (2% oxygen) for 24 hours, and intracellular levels of adenosine were determined by HPLC (*P < .05). (B) Confluent HMEC-1s were treated with indicated concentrations of the AK inhibitor 5′-iodotubericidin (ITU) over 30 minutes, and intracellular levels of adenosine were determined by HPLC (*P < .01). (D) HMEC-1 cells were treated with indicated concentrations of ITU and Ado transport was quantified. Control experiments were performed in the presence of dipyridamole (20 μM). Measurements were performed in triplicate (mean ± SD). Shown is 1 of 3 representative experiments.

Adenosine kinase (AK) in modulating intracellular adenosine concentration and adenosine uptake. (A) Confluent HMEC-1s were exposed to normoxia or hypoxia (2% oxygen) for 24 hours, and intracellular levels of adenosine were determined by HPLC (*P < .05). (B) Confluent HMEC-1s were treated with indicated concentrations of the AK inhibitor 5′-iodotubericidin (ITU) over 30 minutes, and intracellular levels of adenosine were determined by HPLC (*P < .01). (D) HMEC-1 cells were treated with indicated concentrations of ITU and Ado transport was quantified. Control experiments were performed in the presence of dipyridamole (20 μM). Measurements were performed in triplicate (mean ± SD). Shown is 1 of 3 representative experiments.

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