Skip to main content
. 2017 Aug 31;113(14):1776–1788. doi: 10.1093/cvr/cvx175

Figure 5.

Figure 5

Cgnl1 silencing disrupts Ve-cadherin association with the actin cytoskeleton. (A) Intracellular staining of HUVECs for Cgnl1 (green signal), DAPI (blue signal) and actin cytoskeleton filaments (red signal), arrowhead indicates Cgnl1 signal colocalized with actin fibers in filopodia during interaction with neighbouring cells. Immunostaining using a species-matched isotypic control validated Cgnl1 signal specificity, as shown in the third column. Micrographs are depicted at 40 × (first two columns), and 20× magnification (third column) (n = 4). (B) Cgnl1 protein levels in HUVECs in the Triton-X insoluble fraction (the actin cytoskeleton associated compartment) versus the soluble fraction. Shown are representative Western blots for β actin and Cgnl1 (left). Graphs show quantified results (right). Values represent mean integrated optical density (IOD) ± SD corrected for β actin loading controls. *P < 0.05 versus soluble (n = 3). Student’s t-test. (C and D) Western blot results show Ve-cadherin protein level in the Triton-X soluble and insoluble fraction in siCgnl1-treated confluent HUVEC monolayers versus sisham or non-treated controls. Graphs show quantified results. Values represent mean IOD ± SD corrected for β actin loading controls. *P < 0.05 versus sisham and control (n = 4). One-way ANOVA.