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. 2016 Sep 10;6(12):2068–2083. doi: 10.7150/thno.15007

Figure 1.

Figure 1

miR-433 is increased in cardiac fibrosis. A, dysregulated miRNAs in hearts from 21 days post-myocardial infarction (MI) versus sham control mice (n=4); B, upregulated miR-433 in ventricle samples from 21 days post-MI mice (n=4), a rodent model of doxorubicin (Dox)-induced cardiomyopathy (n=6), and human dilated cardiomyopathy (n=4); C-D, increased miR-433 in two in vitro cardiac fibrosis model induced either by TGF-β or Angiotensin II (n=6); E, expression of miR-433 in neonatal cardiac fibroblasts (NRCF) compared to cardiomyocytes (NRCM) (n=6); F, markers for pathological hypertrophy (ANP, BNP and Myh7) and extracellular matrix proteins (CTGF, TSP-1, Col1a1 and Col3a1) in cardiomyocytes with miR-433 overexpression (n=6). Scale bar: 50 μm. *, P<0.05, **, P<0.01, ***, P<0.001 versus respective controls.