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To ensure that we did not introduce a bias due to possible differences in cell viability in response to an inflammatory stimulus, we examined viability using calcein AM, which produces an intense fluorescence in live but not dead cells (Figure?S2). We found no significant differences in viability after LPS treatment (p?= 0.76) between cells from strains included (93.6%) and strains not included in this study (94.9%). In a genetically diverse population such as our panel of strains,?GxE interactions can be observed when a strain(s) responds to a given environmental stimulus (e.g., LPS), whereas another strain(s) of different genetic background does not. We found GxE interactions in 2,607 (20.1%) genes in LPS-treated cells, 512 (3.9%) genes in OxPAPC-treated cells, and 2,786 (21.5%) genes that showed a GxE interaction in at least one of the conditions. Although click here treatment influenced expression levels in a larger number of genes for LPS than Bumetanide for OxPAPC treatment, a large proportion of the genes differentially expressed show GxE interactions in both LPS (2607/2802, 93%) and OxPAPC (512/593, 86%) treatments. The total number of genes regulated and genes regulated over 2-fold is shown in Table S1. Figure?1 shows representative examples of environmental, genetic, and GxE effects. Expression levels of Heme Oxygenase-1 (Hmox1) are shown in Figure?1A for cells in control and OxPAPC-treated cells in different mouse strains and in Figure?1B for cells in control and LPS-treated cells. Hmox1 expression is strongly regulated by environmental inflammatory stimuli in response to OxPAPC (p?ABT-199 solubility dmso receptor signaling (p?= 4.1 x 10?6) were highly enriched in response to LPS, whereas regulation of kinase activity (p?= 4.7 x 10?5), cytokine production (p?= 3.7 x 10?5), and SH2 domain (p?= 1.8 x 10?4), which recognizes phosphorylated tyrosine residues, were enriched in response to OxPAPC. Genes that were regulated by OxPAPC and not by LPS were enriched in glutathione metabolism (p?= 1.5 x 10?5) and response to oxidative stress (p?= 9.5 x 10?3), consistent with the hypothesis that oxidative stress plays a major in role in chronic inflammatory disorders such as atherosclerosis.