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. Author manuscript; available in PMC: 2015 Apr 20.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Jun 20;33(8):1911–1919. doi: 10.1161/ATVBAHA.113.301591

Figure 3.

Figure 3

Mitochondrial oxidative stress and dysfunction inhibit tube formation on 2D Matrigel in human coronary artery endothelial cells (HCAECs). HCAECs were treated with vehicle (A), vascular endothelial growth factor (VEGF; 50 ng/mL; B), rotenone (Rot; 1 µmol/L; C), and Rot/VEGF (D). Bar graph summarizing the number of tubes formed under each condition is shown in E. Although VEGF induced robust formation of tubes on 2D Matrigel, Rot inhibited this process in the presence or absence of VEGF (*P<0.05; n=4; 8–12 wells/condition), implying that mitochondrial bioenergetics is the upstream regulator of growth factor–mediated signaling cascade.