Fig. 1: Peli1 knockout ameliorates TAC-induced cardiac hypertrophy. | Cell Death & Disease

Fig. 1: Peli1 knockout ameliorates TAC-induced cardiac hypertrophy.

From: HNF4α ubiquitination mediated by Peli1 impairs FAO and accelerates pressure overload-induced myocardial hypertrophy

Fig. 1

8-week-old WT and Peli1KO mice were randomly subjected to transverse aortic constriction (TAC) or sham surgery for 4 weeks. A, B Western blot analysis of Peli1 in the left ventricular myocardium, GAPDH as the loading control. (n = 6). C Representative gross morphology of hearts (n = 12 for WT sham group, n = 14 for WT TAC group, n = 6 for KO sham group and n = 10 for KO TAC group). Scale bar: 2 mm. D–F Heart weight-to-body weight (HW/BW) ratio (D), heart weight-to-tibia length (HW/TL) ratio (E), and lung weight-to-body weight (LW/BW) ratio (F) (n = 12 for WT sham group, n = 14 for WT TAC group, n = 6 for KO sham group and n = 10 for KO TAC group). G Representative graphs of H&E staining (top) and WGA staining (bottom). (n = 6). Scale bar: 40 μm. H Cross sectional area of cardiomyocytes counted by WGA staining. (n = 6). I–K qRT-PCR was performed to analyze the mRNA levels of atrial natriuretic peptide (ANP) (I), brain natriuretic peptide (BNP) (J), and myosin heavy chain beta (β-MHC) (K) (n = 12 for WT sham group, n = 14 for WT TAC group, n = 6 for KO sham group and n = 10 for KO TAC group). Values are mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 (one-way ANOVA followed by Tukey’s test).

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