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. 2021 Feb 15;10(5):e018913. doi: 10.1161/JAHA.120.018913

Figure 4. Knockdown of TIGAR ameliorated the HG‐induced ROS formation and apoptosis, promoted angiogenesis in ECs cocultured with cardiomyocyte conditioned media.

Figure 4

A, Dihydroethidium staining revealing that knockdown of TIGAR ameliorated the HG‐induced ROS formation. All data represent mean±SD (n=3 per group, **P<0.01). B, Representative images and quantification of TUNEL+ cells. Knockdown of TIGAR decreased the HG‐induced TUNEL+ cells numbers (green, ×20). All data represent mean±SD (n=5 per group, **P<0.01). C, Knockdown of TIGAR significantly increased total branching length compared with HG media treatment. All data represent mean±SD (n=3 per group, **P<0.01). D, Migration of PAECs was assessed using a scratch wound assay. Migration in distance was significantly decreased in the HG media treatment group, while knockdown of TIGAR significantly increased PAEC migration rate compared with HG media treatment. All data represent mean±SD (n=5 per group; **P<0.01). HG indicates high glucose; PAEC, pig artery endothelial cells; ROS, reactive oxygen species; TIGAR, TP53‐induced glycolysis and apoptosis regulator; and TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.