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Adenosine A2A Receptor Deletion Enhances Neointimal Formation from Arterial Injury in Apolipoprotein‐E Deficient Mice

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is caused by neointimal proliferation due to vascular inflammation in response to arterial injury. The adenosine A2A receptor (A2AR) has an anti‐inflammatory effect in various mouse inflammatory disease models. Hence, we investigated whether A2AR activation influences neointimal formation using a mouse carotid artery wire injury model. A2AR deficient (A2AR−/−) mice were crossed with apolipoprotein‐E deficient (apoE−/−) mice to generate double knockout mice. These mice and their littermate controls were fed a western diet for 2 weeks, followed by wire injury to their left carotid arteries. Four weeks after arterial injury, Movat’s pentachrome was used to stain cross‐sections of carotid arteries to assess overall features of neointimal hyperplasia. We found that A2AR deletion in apoE−/− mice increased the size of neointima by 6 fold over apoE−/− mice (P<0.01) after arterial injury. This study demonstrates that the A2AR plays a significant role in the formation of arterial neointima and suggests that A2AR agonists may be useful to inhibit restenosis after PTCA.