Abstract 133: Nicotine Treatment Changes the [18F]FDG and [18F]2FA Uptake Level to Cultured Macrophages
Objectives: It is well known that smoking is one of the risk factors for atherosclerosis, and previous reports have shown that nicotine induces cytokine release in cultured macrophages and stimulates plaque growth in a mouse model of atherosclerosis. We and other group have shown that a glucose metabolism imaging probe for PET, [18F]FDG, can specifically detect vulnerable plaque depending on the macrophage infiltration extent. In this study, we investigated the effects of nicotine on [18F]FDG uptake in cultured macrophages. In addition, the uptake study was also performed with α4β2 nicotine receptor imaging agent, [18F]2FA.
Methods: Macrophages were isolated from mice peritoneum following thioglycollate injection, and cultured for 24hrs. Then, nicotine was added to each culture well at the concentration of 0, 0.1, 1 or 10 μM. After the culture for 24 hrs, [18F]FDG or [18F]2FA was added to each well and incubated for 1hr at 37°C. Then, the cells were peeled from each well and the radioactivity was measured. The protein concentration was measured by Lowry’s method.
Results: [18F]FDG uptake to the cells were 5.6 ± 0.8, 7.7 ± 2.3, 8.1 ± 1.8 and 8.7 ± 2.3 %dose/mg protein at 0, 0.1, 1 and 10 μM nicotine, respectively. The significantly higher uptake was observed in 1 and 10 μM nicotine treated groups compared to untreated group (0μM). [18F]2FA uptake was higher in 10μM nicotine treated group than untreated group.
Conclusions: Our results show that macrophage metabolic activity was activated by nicotine, and nicotine α4β2 receptor up-regulation was induced by nicotine treatments. Further investigation with α7 nicotinic receptor imaging agent is undergoing to elucidate the relationship between nicotinic receptor and atherosclerosis.
- © 2012 by American Heart Association, Inc.