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. 2014 Apr 25;3(2):e000434. doi: 10.1161/JAHA.113.000434

Figure 7.

Figure 7.

MicroR‐23b (miR‐23b) directly targets CA‐II expression and modulate myocyte hypertrophy and death in vitro. A, miR‐23b precursor transfection increased miR‐23b levels in nCMs and arCMs in vitro compared with miR‐scrambled precursor (CON); *P<0.001 vs CON. B, Effects of normal/low glucose (CON), high glucose (HG), ETZ, miR‐23b precursor, and anti–miR‐23b on nCM hypertrophic growth assessed by [3H]leucine incorporation; *P<0.03 vs CON, ETZ, miR‐23b, HG+miR‐23b, and anti–miR23b+ETZ. When not specified, drug treated or transfected cells were grown in normal/low glucose. C, Effects of normal/low glucose (CON), high glucose (HG), ETZ, miR‐23b precursor, and anti–miR‐23b on ANF, BNP, and β‐MHC mRNA levels in nCMs in vitro; *P<0.03 vs CON, ETZ, miR‐23b, HG+miR‐23b, and anti–miR23b+ETZ. D, Effects of normal/low glucose (CON), high glucose (HG), ETZ, miR‐23b precursor, and anti–miR‐23b on arCM apoptotic death in vitro; *P<0.01 vs CON, ETZ, miR‐23b, HG+miR‐23b, and anti–miR23b+ETZ. E, mRNA levels of CA‐II in nCMs cultured in low/normal glucose (CON) or high glucose (HG) and transfected with miR‐23b precursor or anti–miR‐23b; *P<0.001 vs CON; #P<0.03 vs all. F, Luciferase activity of wild‐type (WT) and mutant (Mut) CA‐II 3′‐UTR sequences separately co‐transfected with miR‐23b precursor or anti–miR‐23b into C2C12 myoblasts. *P<0.01 vs all. G, Effects of normal/low glucose (CON), high glucose (HG), miR‐23b precursor, and a mutant CA‐II construct (lacking the 3′‐UTRs, CA‐IImut) on nCM cell size in vitro; *P<0.003 vs all, #P<0.03 vs HG. All quantitative data are from 4 independent experiments. Quantitative data are expressed as mean±SE. arCM indicates adult ventricular cardiomyocyte; EZT, 6‐ethoxyzolamide; nCM, neonatal cardiomyocyte; UTR, untranslated region.