Sustained pharmacological inhibition of δPKC protects against hypertensive encephalopathy through prevention of blood-brain barrier breakdown in rats
J. Clin. Invest. Xin Qi, et al. 118:173 doi:10.1172/JCI32636 [Go to this article.]

Figure 4
Sustained δV1-1 treatment preserves the integrity of the cerebral capillaries of hypertensive rats. Brain cortex samples were collected from 13-week-old DS rats treated with either TAT or δV1-1 and stained with δPKC using the immunogold labeling method. (A) Middle: δPKC immunogold labeling in endothelial cells and improved morphology of basal lamina (BL) after δV1-1 treatment were noted. L, vessel lumen. A scheme of the area studied is shown at left; a histogram depicting quantitative data of gold particles in endothelial cells is shown at right. Data are mean ± SEM (n = 3 animals per group). F = 16.75, df = 2. *P < 0.05 versus TAT treatment; ^#P < 0.05 versus normotensive rats. (B) Increased δPKC levels in the endfeet of astrocytes (AS) that envelop vessel walls were seen in rat brains from hypertensive rats, which were blocked by δV1-1 treatment. (C) Immunohistochemical analysis of astrocytes surrounding cerebral vessels. Frozen sections of rats treated with TAT or δV1-1 were stained with AQP4, a marker of astrocyte endfeet process. Immunostaining of AQP4 around the cerebral vessel wall was observed. n = 3 rats per group.