Is expression of VEGF isoforms by epiphyseal chondrocytes during low-oxygen tension HIF-1 alpha dependent?
The data presented here clearly indicate that hypoxia is able to induce the synthesis of soluble VEGF isoforms by epiphyseal chondrocytes, most likely through stabilization of HIF-1 alpha. Thus it can be speculated that HIF-1 alpha is an essential prerequisite for hypoxic VEGF synthesis in the epiphysis, thereby contributing to the formation and invasion of blood vessels in long bone development.
This study suggests that VirS is required for VapA expression and that regulation of PvapA-promoter activity may be achieved by controlling VirS expression levels.