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. 2018 Jan 25;41(4):1909–1916. doi: 10.3892/ijmm.2018.3428

Figure 3.

Figure 3

Cardiac hypertrophy is attenuated and ventricular function is preserved by miR-327 inhibition after TAC surgery. (A) Decreased miR-327 in hearts of mice treated with miR-327 antagomiR as determined by RT-qPCR (n=6). (B) Representative images of isolated mouse hearts (scale in mm). (C) miR-327 inhibition attenuated the HW/BW and HW/TL ratios (n=6). (D and E) Echocardiograms indicated that miR-327 inhibition preserved EF and attenuated LVPW and LV mass (n=6). (F) Histological examination indicated that miR-327 inhibition reduced cardiac hypertrophy and fibrosis (n=3; scale bar, 500 µm in the top panel and 50 µm in the others). (G and H) Western blot analysis revealed that miR-327 inhibition prevented the phosphorylation of MAPK proteins (n=3). (I) miR-327 inhibition caused a downregulation of fibrosis-associated genes in mice (n=6). ##P<0.01, ###P<0.001 vs. respective Sham + NC antagomiR; *P<0.05, **P<0.01, ***P<0.001 vs. respective TAC + NC antagomiR. ns, no significance; nc, negative control; col, collagen; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; miR, microRNA; TGF, transforming growth factor; TAC, transverse aortic constriction; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; EF, ejection fraction; HW, heart weight; BW, body weight; TL, tibia length; LVPW, left ventricular posterior wall; MAPK, mitogen-activated protein kinase; TGF, transforming growth factor.