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. 2016 Oct 4;24(11):1939–1948. doi: 10.1038/mt.2016.166

Figure 2.

Figure 2

Genetic deletion of miR-21 in nonmyocyte cells preserves cardiac function in a cardiac disease model. Echocardiography in mice with global genetic deletion of miR-21 (miR-21-/-) or in mice where deletion was targeted to cardiac myocytes or nonmyocytes upon infecting miR-21fl/fl mice with iCre-encoding AAV9 or MMLV, respectively. Controls for these groups were wildtype (WT) or dsRed-encoding vectors. Mice were either subjected to transverse aortic constriction (TAC) or received sham surgery as a negative control. (a) Experimental strategy. (b) Representative recordings from TAC-treated mice with global or targeted miR-21 deletion. (c) Quantification of the left ventricular ejection fraction in TAC- or sham-operated mice from the above approaches. Green, blue, and orange color codes are used for groups with global, CM- or non-CM-targeted deletion of miR-21, respectively, with darker color for the genetically manipulated mice and brighter color for their genetic controls. (d) Left ventricular volume (LV volume) in the above groups. miR-21 global deletion mice Sham n = 9, TAC n = 16–18. AAV9- Ctrl/-iCre Sham n = 6–7; TAC n = 5–9. MMLV-Ctrl/-iCre Sham n = 6–9; TAC n = 7–8. Data are mean ± SEM. and were analyzed using two-way analysis of variance (ANOVA) with Sidak's post-test. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. AAV9, adenoassociated virus of serotype 9; CM, cardiac myocytes; iCre, improved Cre recombinase; MMLV, moloney murine leukemia virus.