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. 2023 Sep 1;24(17):13571. doi: 10.3390/ijms241713571

Figure 3.

Figure 3

Transcriptomic profiling indicates that 17 β-estradiol blocks TNFα-NF-κB signaling and inflammation (A) Principle component analysis plot from RNAseq performed on aortic root tissue of male wild-type (n = 5), Marfan (n = 5), Marfan treated with eight weeks of 17 β-estradiol (n = 5), and seven days of angiotensin II treated wild-type (n = 4), Marfan (n = 4), and Marfan mice treated with five weeks of 17 β-estradiol (n = 4). (B) Gene enrichment analysis of the hallmark gene set TNFα signaling via NF-κB comparing Marfan mice to a cohort of combined wild-type and Marfan mice treated with 17 β-estradiol (left). The same analysis in angiotensin II treated mice (right). (C) Dot plot of transcription factors with targets enriched in Marfan mice compared to Marfan mice with 17 β-estradiol using the TRRUST database (top). The same analysis was in angiotensin II-treated mice (bottom). (D) Normalized read counts of Mcp-1, Vcam-1, Lgasl3, Il-6, Cxcr4, and Cxcl5 gene expression from the same mouse cohorts outlined in (A). Box plots describe quartiles. Adjusted p-values from DESeq2 for pairwise comparisons are depicted in charts. AII: angiotensin II, E2: 17 β-estradiol, MFS: Marfan syndrome, WT: wild-type.