Reactive oxygen species-driven HIF1 α triggers accelerated glycolysis in endothelial cells exposed to low oxygen tension

Endothelial cells and their metabolic state regulate glucose transport into underlying tissues. Here, we show that low oxygen tension stimulates human umbilical vein endothelial cell 18F-fluorodeoxyglucose (18F-FDG) uptake and lactate production. This was accompanied by augmented hexokinase activity and membrane Glut-1, and increased accumulation of hypoxia-inducible factor-1 α (HIF1α). Restoration of oxygen reversed the metabolic effect, but this was blocked by HIF1α stabilization. Hypoxia-stimulated 18F-FDG uptake was completely abrogated by silencing of HIF1α expression or by a specific inhibitor.

Source: Nuclear Medicine and Biology - October 25, 2016 Category: Nuclear Medicine Authors: Jin-Young Paik, Kyung-Ho Jung, Jin-Hee Lee, Jin-Won Park, Kyung-Han Lee Source Type: research