Fig. 2 | Laboratory Investigation

Fig. 2

From: OxHDL controls LOX-1 expression and plasma membrane localization through a mechanism dependent on NOX/ROS/NF-κB pathway on endothelial cells

Fig. 2

In vivo oxHDL administration increases LOX-1 expression at the endothelial cellular plasma membrane. Rats were intraperitoneally treated with vehicle (a, d, g and j), HDL (b, e, h and k), and oxHDL (c, f, i and l) for 24 h. After treatment, the aorta (ac), renal artery (df), renal vein (gi), and hepatic vein (jl) were extracted and subjected to fluorescence immunohistochemistry to determine LOX-1 (green) expression. Immunohistochemistry was also performed using the endothelial protein VE-Cadherin (red). Nuclei were stained with Hoechst (Sigma). Scale bar = 50 μm. Representative images from western blot experiments performed to detect LOX-1 in the plasma membrane-rich fraction in RMECs from vehicle-treated, HDL-treated, and oxHDL-treated rats (m). Densitometric analyses of (m) are shown in (n). The protein levels were normalized against the Na+ pump. The data are expressed normalized to the vehicle condition (N = 3). Statistical differences were assessed using one-way analysis of variance (ANOVA) (Kruskal–Wallis), followed by Dunn’s post-hoc test. **P < 0.01. Graph bars show the means ± SD. Ox-HDL-induced Oct-1 (o) and NF-κB-p50 (p) mRNA expression was determined by RT-qPCR in RMECs from vehicle-treated, HDL-treated, and oxHDL-treated rats. The data are expressed normalized to the vehicle condition (N = 3). Statistical differences for HAEC and HUVEC samples were assessed by one-way analysis of variance (ANOVA) (Kruskal–Wallis) followed by Dunn’s post-hoc test. **P < 0.01. Graph bars show the means ± SD

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