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Objective— The A2B adenosine receptor (A2B R) is highly expressed in macrophages and vascular smooth muscle cells and has been established as an important regulator of inflammation and vascular adhesion. Recently, it has been demonstrated that A2B R deficiency enhances neointimal lesion formation after vascular injury. Therefore, we hypothesize that A2B R agonism protects against injury-induced intimal hyperplasia.Methods and Results— Apolipoprotein E–deficient mice were fed a Western-type diet for 1 week, after which the left common carotid artery was denuded. Mice were treated with the A2B receptor agonist BAY60-6583 or vehicle control for 18 days. Interestingly, lumen stenosis as defined by the neointima/lumen ratio was inhibited by treatment with the A2B receptor agonist, caused by reduced smooth muscle cell proliferation. Collagen content was significantly increased in the BAY60-6583–treated mice, whereas macrophage content remained unchanged. In vitro, vascular smooth muscle cell proliferation decreased dose dependently whereas collagen content of cultured smooth muscle cells was increased by BAY60-6583.Conclusion— Our data show that activation of the adenosine A2B receptor protects against vascular injury, while it also enhances plaque stability as indicated by increased collagen content. These outcomes thus point to A2B receptor agonism as a new therapeutic approach in the prevention of restenosis.

Adenosine A2BReceptor Agonism Inhibits Neointimal Lesion Development After Arterial Injury in Apolipoprotein E–Deficient Mice

Adenosine A_2BReceptor Agonism Inhibits Neointimal Lesion Development After Arterial Injury in Apolipoprotein E–Deficient Mice