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Fig. 3 | Clinical Epigenetics

Fig. 3

From: Apabetalone (RVX-208) reduces vascular inflammation in vitro and in CVD patients by a BET-dependent epigenetic mechanism

Fig. 3

Apabetalone does not interfere with NF-kB translocation from the cytoplasm to the nucleus or association of RelA with the chromatin shown via western blot and ChIP. a Western blot: Phospho-RelA and total-RelA is found almost exclusively in the HUVEC cytoplasm (C) under unstimulated conditions (DMSO). b TNFα stimulation induces phospho-RelA and total-RelA translocation to the nucleus (N). c Apabetalone (20 μM) co-treatment (2 h) does not alter translocation. a–c The loading control used was β-actin, the nuclear protein control was BRD2 and cytoplasmic control was α-tubulin. d ChIP: RelA occupancy on the VCAM1 enhancer and promoter, the SELE enhancer and promoter, and the promoters of MCP-1 and IL-8 increases substantially with TNFα stimulation. Apabetalone (5 and 20 μM) does not reduce RelA occupancy. e BRD4 occupancy on the VCAM1 enhancer and promoter, the SELE enhancer and promoter, and the promoters of MCP-1 and IL-8 also increases substantially with TNFα stimulation. Apabetalone (5 and 20 μM) diminishes BRD4 occupancy at each of these sites. ChIP locations from transcriptional start sites are indicated by the target gene. Statistical significance was determined through 1-way ANOVA analysis followed by Dunnett’s Multiple Comparison Test using TNFα response for the comparison, where *p < 0.05, **p < 0.01, ***p < 0.001

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