Figure 7.
mir-155 Deficiency Increases Fibroblasts Proliferation and Decreases Inflammation
(A) Western blotting analysis and quantification of Sos1 expression in the heart of infarcted WT and mir-155−/− mice (n = 9 per group). *p < 0.05 versus WT mice after MI. (B) Shown is BrdU staining and quantification of BrdU positive cells of proliferative cells in infarcted heart (n = 3 per group). *p < 0.05 versus WT mice after MI. Scale bar, 100 nm. (C) Western blotting analysis and quantification of Socs1 expression in the heart of infarcted WT and mir-155−/− mice (n = 9 per group). *p < 0.05 versus WT mice after MI. (D) Shown are H&E staining on the infarcted area of WT and mir-155−/− heart tissue 7 days after AMI (n = 9 per group). Scale bar, 100 nm. (E) Real-time PCR analysis of IL-1β, IL-6, TNF-α, and CCL-2 mRNA levels in WT and mir-155−/− mouse hearts (n = 9 for WT mice and n = 11 for mir-155−/− mice). Data are mean ± SEM. Paired t test was used. *p < 0.05 versus WT mice after MI. (F) Western blotting analysis and quantification of Sos1 and Socs1 expression in the heart of mir-155−/− mice transfused with AngII-stimulated mir-155−/− Mφ-secreted exosomes (exoAngII-KO Mφ) or AngII-stimulated WT Mφ-secreted exosomes (exoAngII-WT Mφ). n = 3 per group. *p < 0.05 versus exoAngII-KO Mφ. (G) Shown is the IL-1β, IL-6, TNF-α, and CCL2 relative folds to GAPDH expression in the heart of mir-155−/− mice transfused with AngII-stimulated mir-155−/− Mφ-secreted exosomes (exoAngII-KO Mφ) or AngII-stimulated WT Mφ-secreted exosomes (exoAngII-WT Mφ) (n = 3 per group). Data are mean ± SEM. Paired t test was used. *p < 0.05 versus exoAngII-KO Mφ.