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. Author manuscript; available in PMC: 2011 Feb 26.

Published in final edited form as: Biochem Biophys Res Commun. 2010 Jan 25;393(1):66–72. doi: 10.1016/j.bbrc.2010.01.080

eNOS acetylation: A) HUVECs were treated with CSE (0.5% and 1.0%) and H₂O₂ (50 and 100 μM) for indicated time points. B) and C) Histograms represent the relative intensity of acetylated lysine levels of eNOS compared to respective controls (n=3). SIRT1 regulation of eNOS acetylation: D) HUVECs cells were pre-treated with or without SIRT1 activator (resveratrol, 10 μM) and inhibitor (splitomicin, 10 μM) for 1 hr and then treated with CSE (1.0%) for 4 hr. E) and F) Histograms represent the relative intensity of acetylated lysine levels of eNOS compared to respective controls (n=3). IgG was used as an isotype control. Data shown are Mean ± SE. **P < 0.01, ***P < 0.001 vs. control groups. ⁺⁺⁺P < 0.001 vs. CSE treatment alone.

eNOS acetylation: A) HUVECs were treated with CSE (0.5% and 1.0%) and H₂O₂ (50 and 100 μM) for indicated time points. B) and C) Histograms represent the relative intensity of acetylated lysine levels of eNOS compared to respective controls (n=3). SIRT1 regulation of eNOS acetylation: D) HUVECs cells were pre-treated with or without SIRT1 activator (resveratrol, 10 μM) and inhibitor (splitomicin, 10 μM) for 1 hr and then treated with CSE (1.0%) for 4 hr. E) and F) Histograms represent the relative intensity of acetylated lysine levels of eNOS compared to respective controls (n=3). IgG was used as an isotype control. Data shown are Mean ± SE. **P < 0.01, ***P < 0.001 vs. control groups. ⁺⁺⁺P < 0.001 vs. CSE treatment alone.