VEGF SIGNALING MECHANISMS IN INCREASED BLOOD BRAIN BARRIER PERMEABILITY FOLLOWING HYPOXIA

Signal transduction mechanisms initiated by VEGF signaling leading to tight junction loss and redistribution of ZO-1 have not been fully elucidated. One potential transducer is vasodilator stimulated phosphoprotein (VASP). Site specific phosphorylation of VASP via PKG at s239 may be critical for tight junction loss in this pathway. Here we demonstrate the localization of VASP to tight junctions and changes in VASP phosphorylation following hypoxia and VEGF signaling. We also demonstrate that theses changes are dependent on VEGFR2 kinas activity. Further studies may give additional insight into molecular targets for modulating BBB integrity.