Abstract
Blood–brain barrier (BBB) dysfunction contributes to the pathophysiology of cerebrovascular diseases such as stroke. In the present study, we investigated the role of PKC isoforms in aglycemic hypoxia-induced hyperpermeability using an in vitro model of the BBB consisting of mouse bEnd.3 cells. PKCβII and PKCδ isoforms were activated during aglycemic hypoxia. CGP53353, a specific PKCβII inhibitor, significantly attenuated aglycemic hypoxia-induced BBB hyperpermeability and disruption of occludin and zonula occludens-1 (ZO-1), indicating a deleterious role of PKCβII in the regulation of BBB permeability during aglycemic hypoxia. Conversely, rottlerin, a specific PKCδ inhibitor, exacerbated BBB hyperpermeability and tight junction (TJ) disruption during aglycemic hypoxia, indicating a protective role of PKCδ against aglycemic hypoxia-induced BBB hyperpermeability. Furthermore, disruption of TJ proteins during aglycemic hypoxia was attenuated by PKCβII DN and PKCδ WT overexpression, and aggravated by PKCβII WT and PKCδ DN overexpression. These results suggest that PKCβII and PKCδ counter-regulate BBB permeability during aglycemic hypoxia.
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