Fig. 4.

Deletion of miR-29 in cardiac myocytes in vivo protects from cardiac remodeling. Tropism of adeno-associated virus 9 for cardiac myocytes in vivo was employed to deliver improved Cre recombinase (AAV9-iCre) to miR-29 b2c ^fl/fl mice for the deletion of this cluster (with miR-29 b2c ^+/+ littermates serving as controls). a Design of the study. 5 × 10¹¹ viral particles (AAV9-iCre) were delivered to 5 day-old mice via intrapericardial injection. Seven weeks later, mice were subjected to TAC or sham surgery and sacrificed another 3 weeks later (after echocardiographic analysis). b Expression of miR-29b and miR-29c in cardiac tissue from mice treated as in a; n = 4–6 mice per group. c Left ventricular fractional shortening as determined by echocardiographic analysis; n = 4–8 mice per group. d (Left) Representative hematoxylin eosin stainings of myocardial sections; scale bar = 2 mm. (Right) Heart weight-to-tibia length ratio; n = 4–11 mice per group. e (Left) Representative myocardial sections stained for fibrosis with Sirius Red/Fast Green and (right) quantitative analysis of the results; n = 4–9 mice per group; scale bar: 2 mm. All quantitative data are reported as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 as determined by Student’s t-test b or two-way ANOVA followed by Bonferroni’s post hoc test c–e