Research Paper Volume 12, Issue 10 pp 9240—9259

BRD4 contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake

Figure 7. BRD4-induced inflammation reinforces the senescent phenotype via paracrine pathways. (A) THP-1 macrophages were cultured with LPS-induced senescent cell-derived conditioned medium for 24 h with or without siBRD4 or the BRD4 inhibitor JQ-1 (1 μM). Representative SA-β-gal was used to detect cell senescence, and Oil Red O staining was used to detect lipid accumulation in the cells. Scale bar, 50 μm. (B, C) The peritoneal macrophages from the Tert-/- mice and human peripheral blood mononuclear cells (PBMCs) were cultured with the corresponding conditioned medium for 24 h. Representative SA-β-gal was used to detect cell senescence, and Oil Red O staining was used to detect lipid accumulation in the cells. Scale bar, 50 μm. The data all represent measured data presented as the mean ± SD. Comparisons between multiple groups were performed using one-way ANOVA, followed by Tukey’s post-hoc test. The experiment was repeated three times. Significant differences among different groups are indicated as **p <0.01 vs. LPS CM; ***p <0.001 vs. Tert-/- CM; ****p <0.0001 vs. LPS-PBMC CM.