Extended Data Fig. 1: Upregulation of cIAP2 post-MI.
From: Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction
a) and b) Gene expression changes within infarcted left ventricle (‘infarct’) are marked at 24- and 48-hours post-MI, as assessed by hierarchical clustering and principal component analyses of the open-source GEO dataset GSE4648. Analyses carried out using Geo2R and the open-source BART bioinformatics tool. c) Differential gene expression patterns identified in 24-hour post-MI ventricle compared with sham control. cIAP2 (Birc3) is significantly upregulated. d) LV infarct region gene expression timecourse of cIAP2 (maroon) and related transcripts cIAP1 (blue) and Xiap (green), contrasted with measured cardiac marker tnnt2 (Cardiac Troponin T) and inflammatory marker cxcl1. e) Compiled expression timecourse of representative myeloid-related transcripts (maroon) and lymphoid transcripts (blue) from LV infarct region post-MI. ptprc (black) = hematopoietic marker gene transcript. f) Gene Ontogeny (GO) pathway enrichment following MI identifies multiple networks requiring cIAP2. g) NOD1−/− mice have reduced systolic dysfunction and cardiac inflammation following MI relative to WT control mice. Control-operated mice: N = 3; MI-operated mice: N = 5. Ejection fraction: N = 4 MI-operated per group. h) cIAP2 is expressed at lower levels, along with inflammatory genes RIPK1, IRAK4 and TRAF6, in multiple danger signaling receptor-deficient mouse models following MI. Image is representative of two similar experiments. Error bars denote Mean +/- SD; p values were calculated using one-way ANOVA with Bonferroni’s correction (g, upper panel) or two-sided t-test (g, lower panel).
