Extended Data Fig. 3: Immune-derived cIAP2 drives inflammation post-MI.
From: Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction
a) Bone marrow chimeric recipient heart and lung weights 28 days post-MI. Controls: N = 5 (WT)/3 (ciap2−/−); MI-operated: N = 17 per group. Results represent aggregate data from three experiments. b) Capillary density (green) of MI infarct border region. Scale bar = 50 μm. N = 4 per group, mean of 3 representative fields per animal. c) Flow cytometric quantitation of heart-infiltrating neutrophils and Ly6Chi monocytes from bone marrow transplanted mice Day 28 post-MI. Control: N = 3; WT chimeric MI: N = 4; ciap2−/− chimeric MI: N = 4. d) Inflammatory cytokine production from splenocytes isolated from bone marrow chimeric mice 28 days post-MI. N = 6 splenocyte cultures/treatment group. e) Left panel: flow cytometric quantitation of lymphocyte populations (CD4 + T cells, CD8 + T cells, B cells) from left ventricle tissue Day 28 post-MI. Right panels: Immunofluorescence microscopy assessing Th17 cell presence (white arrowheads) in left ventricular MI border zone. Green – IL-17A; red – CD3ζ chain; blue – DAPI. 400x magnification; scale bar denotes 50 μm. Cell quantitation was performed in WT: N = 3, ciap2−/−: N = 4, 4 fields counted per animal. Error bars denote Mean +/- SD; p values were calculated using two-way ANOVA with Bonferroni’s correction (a), one-way ANOVA with Bonferroni’s correction (b, c) or two sided t-test (d, e).
