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. Author manuscript; available in PMC: 2016 Nov 6.
Published in final edited form as: Circ Res. 2015 Oct 5;117(11):967–977. doi: 10.1161/CIRCRESAHA.115.306919

Figure 7. Arg1 may mediate the pathological function of FoxO4.

Figure 7

(A) WT mice were given IV vehicle PBS or the arginase inhibitor BEC at one day before, the day of MI, and one day after MI and sham surgeries. The arginase inhibitor had a similar cardioprotective effect post-MI (filled-diamond with solid line vs open-square with solid line) as inactivation of FoxO4 (open-square with solid line in D vs open-square with sold line in A) (n=5–8). *, BEC vs PBS-treated groups following MI. *, p<0.05. (B) mRNA of selective cytokines expressed in RA and IA of post-MI day 1 WT mouse hearts with or without BEC treatment (n=6–7), *, p<0.05, BEC vs PBS-treated groups. (C) FACS profiles of neutrophils from post-MI day 2 WT mouse hearts treated with or without BEC (n=5–7), *, p<0.05. (D) FoxO4 KO mice were given IV PBS or the NOS inhibitor L-NAME as the same time points as (A). The improved cardiac function due to inactivation of FoxO4 over that of WT mice (open-square with solid line in D vs open-square with solid line in A) is significantly reversed by L-NAME (filled diamond with solid line in D) (n=4–5). *, p<0.05. PBS vs L-NAME treated groups after MI.