Figure 7

Plekhm2 deficiency attenuates AngII-induced cardiac hypertrophy in mice. Mice (males) were implanted with Alzet osmotic pumps containing saline (n = 6–7) or Angiotensin-II (AngII; 2 mg/kg/day, n = 7–8) for 2 weeks. Gravimetric analysis of the heart weight/body weight (mg/g) ratio (A) and echocardiographic parameters (B) were both assessed 2 weeks after implantation and revealed cardiac hypertrophy in WT mice in response to AngII. (C) mRNA levels of genes related to cardiac stress: natriuretic peptides A (nppa), myosin heavy chain7 (myh7), actin, alpha skeletal muscle (acta1), and actin, aortic smooth muscle (acta2). (D) Paraffin-embedded sections of whole heart were stained with Masson’s trichrome. Cardiomyocytes are stained in red while the fibrotic area is stained in blue. Fibrosis was calculated as the percentage of the fibrotic area from the total area of the heart section and the results are normalized to WT saline (a). The difference between WT and PLK2-KO mice treated with AngII is emphasized when the results are normalized to saline treatment in each group (b). (E). mRNA levels of genes related to fibrosis: collagen alpha-1(I) chain (col1a1), collagen alpha-2(I) chain (col1a2), collagen alpha-1(XIII) chain (col3a1), and transforming growth factor beta (tgfβ). The results for mRNA levels are displayed as the fold of saline-treated mice (∆CT) due to high variability in the baseline results. Statistical analyses were conducted with GraphPad Prism 6 as described in the Methods. *p < 0.05, **p < 0.01, and ***p < 0.001.