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. Author manuscript; available in PMC: 2024 Oct 1.
Published in final edited form as: Biomaterials. 2023 Jul 13;301:122245. doi: 10.1016/j.biomaterials.2023.122245

Figure 6. BRD4 is an upstream regulator of both DOT1L and AURKB in SMCs.

Figure 6.

A. BRD4 silencing reduces DOT1L expression. Mouse SMCs (MOVAS) were transduced with lentivirus to express scrambled or gene-specific shRNAs. The transduced cells were allowed to recover in fresh medium for 24h and then starved overnight in basal medium prior to stimulation with PDGF-BB (20ng/ml) for 24 h. Immunoblots: Mean ± SEM, n = 3 independent repeat experiments. qRT-PCR: Mean ± SD, n = 3 replicates. ANOVA and Tukey test: *p<0.05, compared to any of the other 3 bars.

B. BRD4 silencing down-regulates AURKB. Rat primary aortic SMCs were transfected with scrambled or BRD4-specific siRNA, and stimulated with PDGF-BB (20ng/ml, 48h). Mean ± SEM, n= 3 independent repeat experiments. Student’s t-test: *p<0.05.

C. BRD4 and H3K27ac co-occupy the genomic region of Aurkb. The data was retrieved by using accession number GSE194390 (see our recent report45). Integrative genomics viewer (IGV) tracks show the comparison of normalized ChIP-seq peaks between injured (+, light color) and uninjured sham-control (-, dark color) arteries. The box on the left highlights the Aurkb TSS region where the binding of H3K27ac and BRD4 increased after arterial injury. Non-specific input indicates low background noise.