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Hung-wen Liu - One of the best experts on this subject based on the ideXlab platform.

Shao-an Wang - One of the best experts on this subject based on the ideXlab platform.

James H Naismith - One of the best experts on this subject based on the ideXlab platform.

F E Parkinson - One of the best experts on this subject based on the ideXlab platform.

  • Effect of adenosine receptor agonists on release of the nucleoside analogue [3H]Formycin B from cultured smooth muscle DDT1 MF-2 cells.
    European journal of pharmacology, 1998
    Co-Authors: S L Borgland, F E Parkinson
    Abstract:

    Adenosine has receptor-mediated effects in a variety of cell types and is predominantly formed from ATP by a series of nucleotidase reactions. Adenosine formed intracellularly can be released by bidirectional nucleoside transport processes to activate cell surface receptors. We examined whether stimulation of adenosine receptors has a regulatory effect on transporter-mediated nucleoside release. DDT1 MF-2 smooth muscle cells, which possess nitrobenzylthioinosine-sensitive (ES) transporters as well as both adenosine A1 and A2 receptors, were loaded with the metabolically stable nucleoside analogue [3H]Formycin B. N6-cyclohexyladenosine (CHA), a selective adenosine A1 receptor agonist, produced a concentration-dependent inhibition of [3H]Formycin B release with an IC50 value of 2.7 microM. Further investigation revealed CHA interacts directly with nucleoside transporters with a Ki value of 3.3 microM. Neither 5'-N-ethylcarboxamidoadenosine (NECA), a mixed adenosine A1 and A2 receptor agonist, nor CGS 21680, a selective adenosine A2A receptor agonist, affected nucleoside release. We conclude that release of the nucleoside Formycin B from DDT1 MF-2 cells is not regulated by adenosine A1 or A2 receptor activation.

  • uptake and release of 3h Formycin b via sodium dependent nucleoside transporters in mouse leukemic l1210 ma27 1 cells
    Journal of Pharmacology and Experimental Therapeutics, 1997
    Co-Authors: S L Borgland, F E Parkinson
    Abstract:

    At least seven functionally distinct nucleoside transport processes exist; however, mouse leukemic L1210/MA27.1 cells possess only one subtype, a Na+-dependent transporter termed N1/ cif . The capacity of this transporter subtype to release nucleosides from L1210/MA27.1 cells was investigated with the poorly metabolized inosine analog [3H]Formycin B. Uptake of [3H]Formycin B into these cells was inhibited by replacement of Na+ in the buffer with choline, or by blocking Na+/K+ ATPase with 2 mM ouabain, inhibiting glycolysis with 5 mM iodoacetic acid or inhibiting nucleoside transport with 1 mM phloridzin. Sodium stimulated uptake with an EC50 value of 12 mM. To measure release of [3H]Formycin B, cells were loaded with [3H]Formycin B (10 μM) then washed and resuspended in buffer. Replacement of Na+ in the buffer with choline enhanced [3H]Formycin B release by 20 to 47%, and significant stimulation of release was observed with Na+concentrations of 30 mM or less. Resuspending loaded cells into Na+ buffer containing 2 mM ouabain or 10 μM monensin, a Na+ ionophore, significantly enhanced [3H]Formycin B release during 20 min by 39% or 29%, respectively. Release of [3H]Formycin B into choline buffer was inhibited 26.5% by 10 mM phloridzin and 39.6% by 10 mM propentofylline, compounds known to inhibit various transporters including Na+-dependent nucleoside transporters. Release was also inhibited significantly by 100 μM concentrations of dilazep, dipyridamole and nitrobenzylthioinosine, inhibitors with selectivity for Na+-independent nucleoside transporters. In the absence of Na+, the permeants adenosine and uridine enhanced [3H]Formycin B release by up to 40.9% and 21.4%, respectively. These data indicate that in the absence of an inwardly directed Na+ gradient, Na+-dependent nucleoside transporters can function in the release of nucleosides.

Leroy B. Townsend - One of the best experts on this subject based on the ideXlab platform.