Figure 4.

EC-targeted KLF11 overexpression preserves the integrity of tight junctions after focal cerebral ischemia. EC-KLF11 Tg mice and WT controls were subjected to 1 h MCA occlusion and 1d or 3d reperfusion. (A-B) Total RNA was extracted from the ipsilateral cortex of EC-KLF11 Tg and WT mice 1d and 3d after MCAO. ZO-1 and occludin mRNA expression levels were determined by qPCR and normalized to cyclophilin (n=6 per group). (C) Total protein was extracted and subjected to gel electrophoresis. The protein levels of ZO-1 and occludin were determined with β-actin as the loading control. (D-E) Quantification of ZO-1 and occludin protein. Experiments were repeated three times and representative blots are displayed. n=6 per group. (F) Representative images and quantification of ZO-1 (green) and occludin (green) on CD31+ microvessels (red) in the cortex of the ischemic hemisphere at 1d after MCAO. (Scale bar: 25 μm.) Endothelial KLF11 overexpression suppressed MCAO-induced disruption of junctional proteins ZO-1 and occludin. n=6 mice per group. * p < 0.05 vs. WT + sham group, # p < 0.05 vs. WT + MCAO group.