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Characterization of ¹⁸F-FDG Uptake in Human Endothelial Cells In Vitro

Department of Nuclear Medicine, Laboratory of Molecular Imaging, Friedrich-Alexander University, Erlangen, Germany

The contribution of ¹⁸F-FDG uptake by endothelial cells to uptake values measured by PET in various tissues is as yet unclear. We therefore sought to characterize ¹⁸F-FDG uptake in an in vitro model of human endothelial cells. Methods: Commercially obtained human umbilical vein endothelial cells (HUVECs) were seeded in 6-multiwell plates 48–96 h before incubation with 1–2 MBq ¹⁸F-FDG per well. Radioactivity measurements were performed after washing and mechanical dissolvation of the cellular monolayers. Cellular ¹⁸F-FDG uptake was referred to protein concentration. This experimental protocol was subsequently varied to study the effect of different parameters of interest. Furthermore, radio-thin-layer chromatography was used to identify intracellular ¹⁸F-FDG metabolites. ¹⁸F-FDG uptake in HUVECs was compared with that by a human monocyte–macrophage (HMM) preparation and by glioblastoma cells (GLIOs) under identical experimental conditions. Results: ¹⁸F-FDG accumulated in HUVECs in a time-dependent manner and was trapped mainly as ¹⁸F-FDG-6-phosphate and ¹⁸F-FDG-1,6-diphosphate. Unlabeled glucose and cytochalasin B competitively inhibited ¹⁸F-FDG uptake, whereas phlorizin had no significant effect. Glucose deprivation significantly enhanced ¹⁸F-FDG uptake by a factor of 2.7, whereas sodium depletion had no significant influence. HUVECs treated with vascular endothelial growth factor (VEGF) showed a significant 82% increase in ¹⁸F-FDG accumulation after a 2-h exposure to 50 ng/mL VEGF. ¹⁸F-FDG uptake in HUVECs was significantly higher than that in HMMs and in the range of the uptake values measured in GLIOs. Conclusion: ¹⁸F-FDG accumulates in HUVECs by mechanisms analogous to those in neoplastic cells or neurons. VEGF significantly stimulates endothelial ¹⁸F-FDG uptake. The observed differences in ¹⁸F-FDG uptake between HUVECs, HMMs, and GLIOs are difficult to extrapolate to in vivo conditions but stimulate further studies on the contribution of endothelial ¹⁸F-FDG uptake to the overall uptake of that tracer in neoplastic or vascular lesions.

Key Words: ¹⁸F-FDG • glucose transport • endothelium • human umbilical vein endothelial cells • vascular endothelial growth factor

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