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Leukocyte adenosine A2A receptor activation inhibits leukocyte‐endothelial interactions in vivo
Author(s) -
Tang Rong,
Wang Huan,
Chen JiangFan,
Linden Joel
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a127
Subject(s) - selectin , chemistry , bone marrow , chemokine , inflammation , receptor , microbiology and biotechnology , adenosine a2a receptor , cell adhesion molecule , immunology , chemokine receptor , intravital microscopy , integrin , in vivo , adenosine receptor , biology , biochemistry , agonist
Adenosine is known to be an important modulator of inflammation. A number of recent studies have demonstrated that many of the anti‐inflammatory effects of adenosine are due to activation of the A2A receptor (A2AR). In this study, we investigated leukocyte‐endothelial interactions in postcapillary venules of the cremaster muscles of wild type, A2AR deficient and bone marrow chimera mice. We found that the number of rolling and adherent leukocytes is much higher in A2AR deficient mice than wild type mice. This was also observed in chimeric mice which wild type mice were reconstituted with A2AR deficient bone marrow cells. Leukocyte‐endothelial interactions in A2AR−/− mice reconstituted with wild type bone marrow were similar to those in wild type mice. Adhesion molecules on A2AR deficient leukocytes, including selectins, selectin receptors, chemokine receptors and integrins, were similar to those on wild type leukocytes. Theses results suggest that leukocyte but not endothelial A2A receptors regulate leukocyte‐endothelial interactions in vivo possibly via receptor‐mediated changes in adhesion molecule function. This work was supported by NIH HL078679, HL080569, and AHA 0430151N to YH and HL47942 to JL.