Figure 2: Overexpression of miR-212 and miR-132 in cardiomyocytes causes hypertrophy and heart failure.
From: The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
(a) Overexpression construct of miR-212/132 under the control of the α-MHC promoter. (b) Expression levels of miR-212 and miR-132 in heart samples of individual wild-type (WT) and miR-212/132 transgenic (TG) mice as assayed by RT–PCR analysis against the mature forms of corresponding microRNAs. Rnu6b was used as housekeeping control. (c) Survival rate of two different miR-212/132 TG mouse families (TG-Fam23, TG-Fam43) versus WT controls was analysed by Kaplan–Meier survival assay (n=87, 65 and 53 for WT, TG-Fam23 and TG-Fam43, respectively). (d) Morphology of explanted hearts from TG and WT mice at 10 weeks after birth. Scale bar, 1 cm. (e,f) Heart-to-body-weight ratios (e) and cardiomyocyte diameter (f) in 8-week-old α-MHC-miR-212/132 transgenic mice compared with their wild-type littermates (n=5–7). Scale bar, 50 μm. (g–i) Echocardiographic analysis of cardiac dimensions and function for α-MHC-miR-212/132 TG mice and WT controls (n=16–18) (g) end-systolic area, (h) end-diastolic area, (i) fractional shortening. All values in e–i represent mean±s.e.m. *P<0.05; **P<0.01; ***P<0.005. DAPI, 4′,6-diamidino-2-phenylindole; WGA, wheat germ agglutinin (membrane stain).
