Figure 1: MiR-212 and miR-132 are pro-hypertrophic miRNAs induced by hypertrophic stimuli.
From: The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
(a) Overexpression of miRNA precursors from a library identified miRNAs enhancing cardiomyocyte growth and brain natriuretic peptide (BNP) secretion. The miRNA family, miR-212/132, is highlighted by red circles. (b,c) Effects of miR-212 and miR-132 precursors and inhibitors (anti) on cardiomyocyte cell size as compared with the effects of scrambled (Scr) controls (n=5–13). Representative images used for quantification of cardiomyocyte cell size are shown in c. (d) Effects of various pro-hypertrophic stimuli on miR-212 and miR-132 expression in neonatal cardiomyocytes (n=6–10). (e) miR-212 and miR-132 expression levels during pressure-induced left ventricular hypertrophy 3 and 21 days after transaortic constriction (TAC) surgery of mice (n=4). (f) Cardiomyocyte diameters after Sham operation or 3, 14 and 35 days after TAC (n=4 per group). (g,h) miR-212 and miR-132 expression (normalized to sno-202 levels) in fractionated cardiomyocytes and cardiac fibroblasts derived from adult mice after 3 and 35 days of TAC. All values represent mean±s.e.m. *P<0.05; **P<0.01; ***P<0.005. Scale bar in c represents 50 μm. ACTN2, α-cardiac actinin; Ang II, angiotensin-2; a.u., arbitrary unit; d, day; DAPI, 4′,6-diamidino-2-phenylindole; FC, fold change; NS, no significant difference; P/I, phenylephrine/isoprenaline.
