Extended Data Fig. 5: Altered myeloid immune cell dynamics in cIAP2−/− mice.
From: Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction
a) (upper panel) cIAP2 upregulation was observed in patient blood leukocyte lysates from MI-sufferers, and not from control or non-MI, heart failure-diagnosed patients. (lower panel) Murine circulating leukocytes demonstrated increased cIAP2 protein expression Day 7 post-MI. b) Quantitation of leukocyte intracellular cIAP1 and cIAP2 protein expression from stable coronary artery disease (CAD) or MI patients using respective enzyme-specific immunoassay (ELISA). Outputs were normalized to whole protein (μg/ml) of cell lysate. N = 6 representative samples per group. c) Representative gating of peripheral blood myeloid (CD11b+) cells Day 3 post-MI. Representative gating d) and quantitation e) of peripheral blood B and T lymphocytes (B cells, CD4+ T cells, CD8+ T cells) from Day 3 post-MI WT and cIAP2−/− mice. f) Measurement of splenic lymphocytes collected 3- and 7- days post-MI. g) Measurement of LV infiltrating lymphocytes collected 7 days post-MI. h) Schematic diagram summarizing cardiac injury inducing leukocyte production and mobilization from the bone marrow and spleen, with subsequent infiltration into the heart being suppressed in the setting of cIAP2 deficiency. Error bars denote Mean +/- SD; p values were calculated using two-sided t-test (a) or one-way ANOVA followed by Bonferroni’s correction (c, d).
