Figures & data
Figure 1. Quantitative analysis of cell death. (A) Flow cytometric data using annexin V/propidium iodide co-staining. (B) Quantitative data obtained from 3 independent experiments. NS = not significant.
Figure 2. Effects of CHH on vascular endothelial permeability. EA.hy926 cells grown in Traswell were exposed to CHH or normoxia for up to 24 h and transendothelial resistance (TER) was measured at various time-points. N = 3 independent experiments for each data point; * = p < 0.05 and ** = p < 0.01 vs. control at the matched time-point; a, b, and c = p < 0.005, p < 001, and p < 0.0005, respectively, vs. basal TER.
Figure 3. Effects of 12-h CHH on VE-Cadherin, PECAM-1 and ZO-1 in EA.hy926 cells. (A) Western blotting of VE-Cadherin, PECAM-1 and ZO-1. (B) Quantitative band intensity using GAPDH as the loading control to normalize. N = 3 independent experiments. (C) Immunofluorescence staining of VE-Cadherin, PECAM-1 and ZO-1 (shown in green) in EA.hy926 cells. Original magnification = 200× for all panels. (D) The mean fluorescence intensity representing protein level was obtained from 10 random high power fields (HPFs) containing at least 100 cells for each conditions.
Figure 4. Effects of 24-h CHH on VE-Cadherin, PECAM-1 and ZO-1 in EA.hy926 cells. (A) Western blotting of VE-Cadherin, PECAM-1 and ZO-1. (B) Quantitative band intensity using GAPDH as the loading control to normalize. N = 3 independent experiments. (C) Immunofluorescence staining of VE-Cadherin, PECAM-1 and ZO-1 (shown in green) in EA.hy926 cells. Original magnification = 200× for all panels. (D) The mean fluorescence intensity representing protein level was obtained from 10 random high power fields (HPFs) containing at least 100 cells for each conditions.
