FIGURE 3.

In vivo augmentation of ¹⁸F-FDG uptake after GM-CSF administration in mice. (A) ¹⁸F-FDG uptake in atherosclerotic mice (n = 30). Animals received siPFKFB3 (n = 10) or scRNA (n = 8) at days 3, 7, 10, and 12 after high-fat/high-cholesterol administration. GM-CSF (37.5 μg/kg; n = 15) or saline (n = 15) was intravenously administered on day 12, and ¹⁸F-FDG and PET analysis was performed on day 14. (B) Aortas were stained with oil red and images evaluated with Image J. (C) Average target and background SUVs from A were compared (n = 15 animals for each group). Target SUVs were higher with than without GMCSF (3.38 ± 0.46 vs. 2.70 ± 0.26; P = 0.046). Background SUVs were unchanged with vs. without GMCSF (0.54 ± 0.10 vs. 0.55 ± 0.10; P = 0.53). (D) In parallel experiment, aortas from untreated (n = 4) or GM-CSF–treated animals (n = 4) as described in A were isolated and RNA extracted for analysis of the indicated genes representative of endothelial cells (F8), smooth muscle cells (Sm22a, Myh11, Col1a1), and macrophages (Lxra). Data are mean ± SD. *P < 0.05 vs. same condition in absence of GM-CSF. ^##P < 0.01 vs. same condition with scRNA. a.u. = arbitrary units; scRNA = scrambled RNA.