Positron Emission Tomography (PET) with 18 F-FGA for Diagnosis of Myocardial Infarction in a Coronary Artery Ligation Model

Figures

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  Figure 1. Quality control of 18F-FGA. (a) and (b) are radio-TLC profiles of 18F-FDG and 18F-FGA, respectively. (c) and (d) are radio-HPLC chromatograms of 18F-FDG and 18F-FGA, respectively.

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  Figure 2. 18F-FGA/PET of MI in mice. Mice belonging to MI, sham, and naïve groups were injected with 300 μCi of 18F-FGA. PET was performed after 1 h. Only MI mice showed uptake in the heart; sham and naïve mice did not show any detectable uptake in the heart.

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  Figure 3. Cardiac SUV of 18F-FGA at various times after MI (mean ± sem; ∗p < 0.05 vs. sham). The lower panel shows representative tomograms of mice imaged after 1 h, 6 h, 1 d, and 3 d after MI.

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  Figure 4. Whole-body images of mice injected with 18F-FGA and 18F-FDG. Approximately 10 MBq of 18F-FGA and 18F-FDG was intravenously injected in normal mice, and PET images were acquired after 30 min of injection. Whereas 18F-FGA rapidly cleared from circulation via the kidneys and did not show any accumulation in the normal heart and brain, 18F-FDG was significantly retained in the heart and brain.

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  Figure 5. Validation of MI model. (a) TTC-stained slices of sham and MI hearts. MI hearts showed significant thinning of the ventricular wall and large areas of unstained necrotic tissue. (b) Cardiac troponin levels in plasma from sham control versus MI mice.

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  Figure 6. Nuclear localization of biotinylated glucaric acid (BGA) in necrotic H9c2 cells. (a) Streptavidin-HRP blot of nuclear fraction. (b) Immunoblots of histone (15 kDa) and actin (43 kDa). (c) Densitometry (DM; n = 3) of two streptavidin-reactive bands.

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  Figure 7. Competition of glucaric acid (GA) with biotinylated glucaric acid (BGA) for binding with nuclear proteins. (a) A representative streptavidin-HRP blot. (b) Densitometry of streptavidin-reactive bands (n = 3).