Research Paper Volume 13, Issue 6 pp 7781—7799

Twist1 signaling in age-dependent decline in angiogenesis and lung regeneration

Twist1-PGC1α signaling controls EC DNA synthesis and migration in young vs. aged ECs. (A) Graph showing EdU-positive young (50 years old) human adipose ECs treated with lentivirus overexpressing PGC1α or Twist1 shRNA (n=5, mean ± s.e.m., *, pB) Graph showing young vs. aged human adipose ECs treated with lentivirus overexpressing PGC1α or Twist1 shRNA migrating towards 5% FBS (n=5, mean±s.e.m., *, pC) Graph showing EdU-positive aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α shRNA, or in combination (n=5, mean ± s.e.m., *, pD) Graph showing aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α shRNA, or in combination migrating towards 5% FBS (n=5, mean ± s.e.m., *, pE) Graph showing EdU-positive aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α, or in combination with VEGFR2 inhibitor SU5416 (n=5, mean ± s.e.m., *, pF) Graph showing aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α, or in combination with VEGFR2 inhibitor SU5416 migrating towards 5% FBS (n=6, mean ± s.e.m., *, p

Figure 3. Twist1-PGC1α signaling controls EC DNA synthesis and migration in young vs. aged ECs. (A) Graph showing EdU-positive young (<50 years old) vs. aged (>50 years old) human adipose ECs treated with lentivirus overexpressing PGC1α or Twist1 shRNA (n=5, mean ± s.e.m., *, p<0.05). As a control, young vs. aged human adipose ECs were treated with lentivirus encoding control shRNA with irrelevant sequences or control virus (vector alone). (B) Graph showing young vs. aged human adipose ECs treated with lentivirus overexpressing PGC1α or Twist1 shRNA migrating towards 5% FBS (n=5, mean±s.e.m., *, p<0.05). (C) Graph showing EdU-positive aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α shRNA, or in combination (n=5, mean ± s.e.m., *, p<0.05). As a control, aged human adipose ECs were treated with lentivirus encoding control shRNA with irrelevant sequences. (D) Graph showing aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α shRNA, or in combination migrating towards 5% FBS (n=5, mean ± s.e.m., *, p<0.05). (E) Graph showing EdU-positive aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α, or in combination with VEGFR2 inhibitor SU5416 (n=5, mean ± s.e.m., *, p<0.05). As a control, aged human adipose ECs were treated with lentivirus encoding control shRNA with irrelevant sequences, control virus (vector alone) or control vehicle. (F) Graph showing aged human adipose ECs treated with lentivirus encoding Twist1 shRNA, PGC1α, or in combination with VEGFR2 inhibitor SU5416 migrating towards 5% FBS (n=6, mean ± s.e.m., *, p<0.05).