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. 2019 Mar 20;9:171. doi: 10.3389/fonc.2019.00171

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Copyright © 2019 Schaaf, Houbaert, Meçe, To, Ganne, Maes and Agostinis.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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CQ treatment, but not ATG5 deficiency, reduces VEGFR2 phosphorylation after VEGF-A stimulation. HUVECs were either (A–D) pretreated with CQ or (E-I) siRNA against ATG5 (siATG5) and treated with 50 ng/ml VEGF-A where indicated. Cells were treated with non-targeting siRNA (siScrambled; siScr) as control. (A,E,I) Cell lysates were analyzed by immunoblotting. (B,F) Graphs display (relative) band intensity ratio of phosphorylated or (C,G) p130 VEGFR2 to p250/p230 VEGFR2. (D,G) Bar graphs display VEGFR1 intensity normalized to GAPDH. (I) HUVECs were cultured in presence or absence of 25 μM CQ for 2 h. A short-term exposure was opted to minimalize any secondary effects on autophagy flux due to CQ treatment. N.D., not detected. (B–D,F–H), n = 3, mean ± SEM.