Abstract
The blood-brain barrier (BBB) is a critical regulator of brain ion homeostasis, and is disrupted in cardiovascular diseases such as stroke. In this study we examined the role of transient receptor potential (TRP) cationic channels in mediating calcium entry and barrier disruption in bEnd3 cells. We used RT-PCR, immunoblotting, fura-2 calcium imaging and functional permeability studies to investigate the involvement of TRPV and TRPC channels in mediating BBB function. Members of the TRPV family, including the flow-sensitive TRPV4, were expressed in BBB endothelial cells. These cells responded to TRPV-specific stimulation, including exposure to phorbol esters and hypo-osmotic stress, with an increase in intracellular calcium that was blocked by ruthenium red, a TRPV family antagonist. Furthermore, in a model of hypoxic stress, ruthenium red prevented hypoxia-induced increase in BBB endothelial cell monolayer permeability. These results suggest a role for TRPV channels, particularly TRPV4, in mediating BBB disruption after stroke. Ongoing studies are investigating the role of flow and TRPV channels in mediating BBB function. (NIH Grant DK070950)
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