Fig. 8: HDAC1-mediated Sp1/Sp3 deacetylation is responsible for captopril-induced AMPKα1/AMPKα2 transcription activation.
From: Endothelial Sp1/Sp3 are essential to the effect of captopril on blood pressure in male mice
A CoIP assay of Sp1 ubiquitination in HUVECs transfected with Flag-Sp1-WT or Flag-Sp1-K703A with different treatments. Quantified analysis of ubiquitin protein level (below). n = 3. B Co-IP analysis of Sp3 ubiquitination in HUVECs transfected with Flag-Sp3-WT or Flag-Sp3-K551R with different treatments. Quantified analysis of ubiquitin protein level (below). n = 3. C, D CoIP assay of C Sp1 and D Sp3 ubiquitination in HUVECs treated with captopril. Quantified analysis of ubiquitin protein level (below). n = 3. E CoIP assay of acetylation levels of Sp1 or Sp3 in HUVECs treated with captopril. Quantified analysis of acetyl-protein level (below). n = 3. F CoIP assay of HDAC1 in HUVECs treated with captopril. Quantified analysis of HDAC1 protein level (below). n = 3. G, H ChIP assay showing the binding of Sp1 or Sp3 to the AMPKα1 (G) and AMPKα2 (H) promoter in HUVECs with different treatments. n = 3. I Relative luciferase activity for the WT constructs of AMPKα1 and AMPKα2 promoter in HUVECs with different treatments. n = 4. Data are presented as mean ± SEM. Two-tailed Student unpaired t test for (E) and (F). One-way ANOVA followed by Bonferroni post hoc analysis for (G–I). Two-way ANOVA followed by Bonferroni post hoc test for (A–D).
