Figure 2.

WWP1 is a driver of cardiac dysfunction and myocardium infarct post-MI. WT mice were treated with rAAV9-cTnT-GFP or rAAV9-cTnT-WWP1 by intravenous injection of tail two weeks before suffering from sham or LAD ligation, and after additional one day, mice were sacrificed. A Infection efficiency was detected by Western blot. n = 3. B-H Cardiac function indices were measured by echocardiography. EF% ejection fraction, FS% fractional shortening, LVEDV left ventricular end-diastolic volume, LVESV left ventricular end-systolic volume, LVIDd left ventricular internal dimension diastole, LVIDs left ventricular internal dimension systole. n = 6. I, J Infarct size was determined by TTC staining and expressed as the percentage of infarct over ventricular areas. n = 3. K-U Mice were treated with rAAV9-cTnT-shScramble or rAAV9-cTnT-shWWP1 by intravenous injection of tail 2 weeks before suffering from sham or LAD ligation, and after additional 3 days, mice were sacrificed. K Immunofluorescence co-staining for cTnI with WWP1 and DAPI in mice hearts infected with rAAV9-cTnT-shScramble or rAAV9-cTnT-shWWP1 at day 3 post-MI. Scale bar = 200 μm. n = 3. L, M WWP1 protein level was detected by Western blots. Corresponding statistic of WWP1 was shown. n = 4. N-T Cardiac function indices were measured by echocardiography. n = 4, 4, 7, 6, respectively. U Infarct size was determined by TTC staining and expressed as the percentage of infarct over ventricular areas. n = 3. The data are shown as the means ± SD. The data shown in A, C-H, J, M, O-T, and U were analysed by one-way ANOVA followed by Bonferroni post hoc test.