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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Exp Hematol. 2009 May;37(5):533–538. doi: 10.1016/j.exphem.2009.02.001

Figure 5.

Figure 5

The A2bAR controls TNF-α levels in macrophages from mice subjected to injury. (A) Peritoneal macrophages were derived form WT mice at one week after femoral artery injury (Injury), or from sham-injured mice (Control), and subjected to measurement of TNF-α release as described under Methods. Each of the values in the control and injury was designated as 1 for normalization within each experimental set. Cells were treated as indicated with vehicle or BAY 60-6583 (1 μM), preceded by a pre-treatment with CVT-6883 (1 μM) or vehicle as described under Methods. TNF-α level is presented as a ratio to the maximal TNF-α level in vehicle-treated cells (designated as 1). Data are averages +/- SD (n=4). *, p < 0.05 for vehicle-treated cells as compared to BAY 60-6583-treated cells, and BAY 60-6583-treated cells as compared to BAY 60-6583 plus CVT-6883-treated cells or just CVT-6883-treated cells. (B) Quantitative PCR analysis of adenosine receptor mRNA levels in macrophages from WT mice after femoral artery injury as compared to sham injury. Adenosine receptor mRNA levels are shown as a ratio to A2aAR mRNA in each mouse. Data are averages +/- SD (n=5). *, p < 0.05 for the A2bAR post injury as compared to sham injury.