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. 2017 Sep 22;22(1):613–627. doi: 10.1111/jcmm.13348

Figure 8.

Figure 8

Schematic diagram depicting the methylation status of the HBS in the VEGF promoter in both WT and AQP4 KO mice, the HIF‐1 binding and the relative VEGF transactivation. In both WT and AQP4 KO mice under normoxia, HIF‐1α is degradated and no VEGF transactivation occurs. In WT mice HIF‐1α is stabilized, interacts with HIF‐1β and binds the demethylated HBS localized in the VEGF promoter. In AQP4 KO mice, despite high levels of HIF‐1α, the absence of HBS demethylation prevents the HIF‐1 binding and the relative VEGF transactivation. Our assumption is that the absence of AQP4 reduces HBS demethylation limiting the accessibility of HIF‐1 to the VEGF gene promoter, therefore reducing VEGF transcription and accumulation in response to hypoxia.