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. Author manuscript; available in PMC: 2017 Jul 22.
Published in final edited form as: Circ Res. 2016 Jun 9;119(3):434–449. doi: 10.1161/CIRCRESAHA.116.308700

Figure 4. Grem2 overexpression attenuates inflammation after MI.

Figure 4

(A) Schematic diagram of the DNA construct used to generate the TGGrem2 transgenic mice. The Grem2 cDNA coding part was cloned behind a fragment of the αMHC (Myh6) gene promoter that specifically directs expression in adult cardiomyocytes. The construct includes the polyadenylation sequences of the human growth hormone gene (hGH PA). (B) qPCR analysis of whole heart RNA samples isolated from WT and TGGrem2 mice at days 0, 2, and 7 post-MI. Induction of endothelial cell-specific membrane proteins E-selectin and Vcam1 is significantly attenuated in TGGrem2 hearts compared to WT. *** P < 0.001; **** P < 0.0001. Two-way ANOVA with Bonferroni multiple comparisons test. N=3 per group for all time points. All data are means ± SEM. (C) Flow cytometry analysis of single cell suspensions of non-cardiomyocyte cells isolated from whole hearts 5 days post-MI shows decreased number of CD45,+ Ly6C+ and F4/80+ cells in TGGrem2 hearts compared to WT. * P < 0.05. Student’s two-tailed unpaired t-test. WT N=6, TGGrem2 N=8. Bars represent means ± SEM. (D) qPCR analysis of whole heart RNA samples isolated from WT and TGGrem2 mice at days 0, 2, and 7 post- MI shows lower fold induction of Tgfβ1 and Il-10 in TGGrem2 hearts compared to WT. ** P < 0.01; *** P < 0.001. Two-way ANOVA with Bonferroni multiple comparisons test. N=3 per group for all time points. All data are means ± SEM.