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Fig. 4 | Stem Cell Research & Therapy

Fig. 4

From: Endothelial progenitor cells transplantation attenuated blood-brain barrier damage after ischemia in diabetic mice via HIF-1α

Fig. 4

Gap formation of TJ in the EPC-treated and PBS-treated diabetic mice after tMCAO. A Representative image of TJ protein occludin (green) and endothelial marker CD31 (red) at12 h and 24 h after tMCAO in the PBS-treated and EPC-treated mice, scale bar = 10 μm. B. Bar graph shows the quantification of gap formation of occludin from figure (A). Data are mean ± SD, n = 6–8 per group. * p < 0.05, EPC-treated vs. PBS-treated mice. C Representative image of TJ protein ZO-1 (green) and endothelial marker CD31 (red), scale bar = 10 μm. D. Bar graph shows the quantification of gap formation of ZO-1 from figure (C). Data are mean ± SD, n = 6–8 per group. * p < 0.05, EPC-treated vs. PBS-treated mice. E Representative image of TJ protein claudin-5 (green) and endothelial marker CD31 (red), scale bar =10 μm. F Bar graph shows the quantification of gap formation of claudin-5 from figure (E). Data are mean ± SD, n = 6–8 per group. * p < 0.05, EPC-treated vs. PBS-treated mice. Western blot analysis shows the occludin (G) and ZO-1 expression (I) in the EPC-treated and PBS-treated mice at 24 h after tMCAO. H and J Bar graphs show the quantitative data of occludin and ZO-1 protein expression. Data are mean ± SD, n = 4 per group. * p < 0.05, EPC-treated vs. PBS-treated mice. EPC endothelial progenitor cell, PBS phosphate-buffered saline

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