Review Volume 8, Issue 12 pp 3180—3184

Figure 1. (A) When iodide exists at normal or sufficient levels in the blood, one iodide ion enters a thyrocyte along with sodium via NIS (sodium-iodide symporter) at the basolateral membrane of the cell. The iodide moves to the apical membrane of thyrocytes along with molecules of hydrogen peroxide. Finally, iodide is oxidized and HIF-1α (hypoxia inducible factor-1α) remains unstable and therefore unable to bind to the VEGF (Vascular Endothelial Growth Factor) promoter. Ultimately, this mechanism reduces the VEGF expression. (B) When iodide exists at insufficient levels in the blood, thyrocytes and thyroid follicles also contain low levels of iodide or no iodide, and cytoplasmic ROS (reactive oxygen species) levels remain high because there is no iodide to be oxidized. These ROS stabilizes HIF-1α, allowing the binding of HIF-1α with HIF-1β, which binds to the VEGF promoter and allows transcription of the VEGF gene.