Fig. 6

Vascular abnormality induced by insufficient Cav-1 is likely mediated by aberrant VEGFR2 and VE-Cadherin. Cav-1, VEGFR2 and VE-Cadherin protein content were assessed in total cell lysates (A, D–F), the soluble fraction B, G and H and the particular fraction C, I and J of Cav-1 depleted HUVECs and controls. Representative images (A–C), as well as quantifications obtained by pixel density assessments, are shown (D–J). Proteins from γ-tubulin, HSP90, and Na/K-ATPase served as loading control for total cell lysate, the soluble, and the membrane fraction, respectively. n = 4. Cav-1, VEGFR2 and VE-Cadherin were assessed in total cell lysates and in biotinylated cell surface proteins of Cav-1 depleted and control ECs (K–P). Representative images K and quantifications obtained by pixel density assessments are shown (L–P). n = 4. Con: control, Cav1 siRNA: Cav-1 depleted, T: total, S: soluble, M: membranous particular. *p < 0.05, **p < 0.01, ***p < 0.001