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 5
Sustained δV1-1 peptide treatment blocks the translocation of ZO-1 and occludin out of the tight junction-enriched cytoskeletal fractions in brains of hypertensive rats. Cytosolic and membranal (detergent-soluble) fractions and cytoskeletal (detergent-insoluble) fraction were isolated from rat brains treated as above. (A) Lysates from DS rat brains were subject to Western blot and analyzed using anti–ZO-1 and anti-occludin antibodies. GAPDH (a cytosolic marker) and Gα (a membranal marker) were used as internal controls. (B) Histogram demonstrating translocation of ZO-1 and occludin out of the cytoskeletonal fractions in TAT-treated rats and its reversal in the δV1-1–treated group. Data are mean ± SEM (n = 3 rats per group). F = 27.97, df = 3 (ZO-1); F = 8.84, df = 3 (occludin). ^#P < 0.05 versus rats fed low-salt diet; *P < 0.05 versus TAT or saline treatment. (C) Total lysates from DS rat brains were subjected to Western blot analysis with anti–ZO-1 and anti-occludin antibodies. GAPDH was used as an internal loading control. n = 3 rats per group.