Research Paper Volume 14, Issue 14 pp 5925—5945

miR-21 upregulation exacerbates pressure overload-induced cardiac hypertrophy in aged hearts

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Figure 4. miR-21 knockout (miR-21−/−) decreased angiotensin II (Ang II)-induced cardiac hypertrophy and fibrosis in both young and aged mice. (A) Representative images of harvested hearts. Quantitative analysis of heart weight/body weight and heart weight/tibia length in wild type (WT) or miR-21−/− of (B) young and (C) aged mice. In WT or miR-21−/− of (D) young and (E) aged mice, representative sections of hearts stained with Masson's trichrome for fibrosis detection (blue); scale bars, 30 μm (left panel). Quantification of cardiac fibrosis (right panel). (F) miR-21−/− decreased Ang II-induced increased cardiac hypertrophy miR-21 expression in primary mouse cardiomyocyte. The representative merged images of light field and F-actin immunofluorescence staining for primary cardiomyocyte isolated from WT and miR-21−/− of young mice. The cell area was measured 100 random cells in each group. The expression of miR-21 was measured by qRT-PCR in each group. *P < 0.05, **P < 0.01, and ***P < 0.001 for difference from each group. (N = 6–8).