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. 2015 Aug 20;19(12):2715–2727. doi: 10.1111/jcmm.12657

Figure 3.

Figure 3

Inhibition of high mobility group box protein 1 (HMGB1) or caspase‐1 activity prevents visfatin‐induced disruption of junction proteins in mouse vascular endothelial cells (MVECs). MVECs were stimulated with or without visfatin (Visf, 4 μg/ml) for 24 hrs in the presence of PBS (Vehl: vehicle), HMGB1 inhibitor glycyrrhizin (GLY, 130 μmol/l) or caspase‐1 inhibitor Z‐WEHD‐fluoromethyl ketone (FMK) (WEHD, 0.2 μg/ml). (A) Immunofluorescence stainings were performed with Alexa555‐conjugated antibodies against ZO‐1, ZO‐2, occludin or VE‐Cadherin (VE‐Cad) for determination of the expression of these junction proteins. Representative images show the cell membrane of fluorescence of ZO‐1, ZO‐2, occludin or VE‐Cadherin (red) are representative of at least three independent experiments. (B–F) Representative Western blot gel document and summarized data showing the protein expression of ZO‐1, ZO‐2, occludin, VE‐Cadherin and β‐actin expression in the microsomes of MVECs (n = 4–5). *P < 0.05 versus Vehl Ctrl; # P < 0.05 versus Visf alone.