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. 2020 Apr 14;30(4):746–765. doi: 10.1111/bpa.12831

Figure 4.

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 and 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 and 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.