Figure 2.

Transfection of lentivirus expressing miR-130a (LmiR-130a) attenuates cardiac dysfunction and decreases collagen deposition after MI. Mice were transfected with LmiR-130a or LmiR-con for 7 days before induction of MI. (A) Increased expression of miR-130a in the myocardium following LmiR-130a transfection. Hearts were harvested at 3 days after MI, sectioned and viewed by fluorescent microscopy. Ischemic areas were collected for miR-130a measurement. (B and C) Cardiac function was examined by echocardiography before (Baseline) and at 1, 3, 7, 14, and 21 days after MI. Transfection of LmiR-130a maintained the levels of ejection fraction (EF%) and fractional shortening (FS%). N=24 in untransfected group. N=11 in LmiR-Control group. N=9 in LmiR-130a group. (D) LmiR-130a transfection decreases infarct size in myocardial ischemia/reperfusion (I/R) injury. Seven days after transfection with LmiR-130a, the mice were subjected to myocardial ischemia (45 minutes) and followed by reperfusion (24 hours). Hearts were harvested for measurement of infarct size by TTC staining. Ratios of risk area vs. left ventricle area (RA/LV) and infarct area vs. risk area (IA/RA) are presented in the graphs. Photographs of representative heart sections are shown above. N=7 in untransfected and LmiR-Control group. N=8 in LmiR-130a group. (E) Increased expression of miR-130a decreases collagen deposition in the myocardium. Three weeks after MI, hearts were harvested for analysis of cardiac fibrosis. Representative images of heart sections stained with Masson's trichrome. N=3 in untransfected and LmiR-Control groups. N=5 in LmiR-130a group. (F) Increased expression of miR-130a attenuates MI-induced increases in the levels of MMP-2 (n=5/group). #p<0.05 compared with LmiR-control and untransfected MI groups at the same time point. *p<0.05 compared with indicated group.