Hypertensive encephalopathy and the blood-brain barrier: is δPKC a gatekeeper?
J. Clin. Invest. Wen-Hai Chou, et al. 118:17 doi:10.1172/JCI34516 [Go to this article.]

Figure 1
Structure of the BBB and tight junction. (A) The BBB is formed in the central nervous system by capillary endothelial cells and surrounding perivascular elements (basal lamina, pericyte, astrocyte end-foot, and interneurons). (B) The tight junction is established by the interaction between the transmembrane proteins (claudins, occludin, and junction adhesion molecule) on adjacent endothelial cells. The C terminal of these transmembrane proteins is linked to cytoskeletal actin through ZO-1. In response to pathological stimuli, δPKC may directly or indirectly increase phosphorylation of ZO-1, thus disrupting the association between ZO-1 and the actin cytoskeleton. The disorganization of proteins at the tight junction may result in the aberrant permeability of the BBB.