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. Author manuscript; available in PMC: 2018 Jun 1.
Published in final edited form as: Exp Hematol. 2011 Feb 12;39(5):525–530. doi: 10.1016/j.exphem.2011.02.004

Figure 4.

Figure 4

MMP-9 levels in macrophages from WT mice after A2bAR activation. (A) Western blotting of vasodilator-stimulated phosphoprotein (VASP) in macrophages treated with BAY 60-6583 (1 µM) or forskolin (2 µM) for 5 minutes. Protein kinase A (PKA) phosphorylates VASP at serine 157 and as a result VASP shifts from 46 to 50 kDa in sodium dodecyl sulfate polyacrylamide gel electrophoresis [24]. The membrane was reprobed with anti–β-actin as loading control. Shown is a representative blot from three experiments. (B) Quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis of MMP-9 mRNA levels, normalized to 18S rRNA in macrophages treated with BAY 60-6583 (1 µM) or forskolin (2 µM) for 2 hours. MMP-9 RNA in vehicle group was used as the reference in relative quantification. Data shown are averages ± standard deviation (SD) (n = 10). *p < 0.05 for vehicle cells as compared to treated cells. (C) Quantitative RT-PCR analysis of MMP-9 mRNA levels, normalized to 18S rRNA in macrophages from TNF-receptor KO mice treated with BAY 60-6583 (1 µM) or forskolin (2 µM) for 2 hours. MMP-9 RNA in vehicle group was used as the reference in relative quantification. Data shown are averages ± SD (n = 5).