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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: J Mol Cell Cardiol. 2015 Oct 13;89(0 0):87–97. doi: 10.1016/j.yjmcc.2015.10.011

Figure 6.

Figure 6

PI3K inhibition abolished the cardioprotective effect of miR-130a following myocardial infarction. (A and B) Transfection of LmiR-130a suppresses PTEN expression and increases the levels of Akt phosphorylation in the presence and absence of MI. Three days after induction of MI, hearts were harvested for analysis of PTEN (A) and phosphorylated Akt (B) levels in the myocardium. N=4 in sham control group. N=6 in MI group. (C-E) PI3K inhibition by LY294004 administration abolished the attenuation of MI-induced cardiac dysfunction by LmiR-130a transfection. (C) EF% and (D) FS% values following MI. N=24 in untransfected group, N=11 in LmiR-Control group, and N=9 in LmiR-130a transfected group. (E) PI3K inhibition by LY294002 abolished LmiR-130a-induced increase in the levels of phosphorylated Akt. N=4-5 in sham control group. N=6 in MI group. * p<0.05 compared with indicated group.