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. 2014 Feb 27;10(2):e1004201. doi: 10.1371/journal.pgen.1004201

Figure 5. CAD-patient macrophage TF-regulatory coexpression networks of PCL-responsive genes linked to atherosclerosis regression.

Figure 5

To learn more about functional interactions of the PCL-responsive gene sets using human orthologs, we used macrophage mRNA profiles (n = 38) from patients with CAD [29] to infer TF-regulatory gene networks. Red square nodes are TFs. Yellow square nodes are specific master regulatory TFs (Table 4): PPARG for the network in early lesions (30 weeks) and MLL5 for the network in mature lesions (40 weeks) and SRSF10 and XRN2 for the network in advanced lesions (50 weeks). Edges are connections between TFs and their first neighbor. (A) At 30 weeks, 53 genes of 215 human orthologs belonged to the TF-regulatory network (P<0.0051), in which the most connected TFs (master regulators) were PPARA (17 edges) and PPARG (13 edges) (Table 2). The TF-regulatory network of PCL-responsive atherosclerosis regression genes at 30 weeks is magnified in (D) to show all nodes. (B) At 40 weeks, 185 genes of 1087 human orthologs in the causal gene set belonged to the TF-regulatory network (P<0.0013). The most connected TFs were HMGB2, ADORA2A, and TERF1, with 61, 59 and 55 edges, respectively (Table 2). (C) At 50 weeks, 379 genes of 1865 human orthologs in the causal gene set belonged to the TF-regulatory network (P<0.00042), in which the most connected TFs were SRSF10, XRN2, and HMGB1, with 71, 67 and 62 edges, respectively (Table 2). (D) A magnification of the TF regulatory network of PCL-responsive genes at week 30, shown in (A).