Fig. 2
Increased β-catenin level restored the normal level of mitophagy and mitigated cardiac hypertrophy in mice with hyperhomocysteinemia. (A) Western blot analyses showed the expressions of protein, including active β-catenin, β-catenin, FUNDC1, LC3II/LC3I, p62 in the hearts of mice subjected to hyperhomocysteinemia in the presence and absence of AAV-β-catenin infection for 4 weeks. (B–F) Quantitative data on active β-catenin, β-catenin, FUNDC1, LC3, p62 proteins in indicated groups. Relative levels of protein were presented as fold induction over the controls. (G) Representative micrographs showed staining for β-catenin and FUNDC1 in the hearts of mice at the end of the 4th week of hyperhomocysteinemia model. Upper panel, immunostaining for β-catenin inthe hearts of mice as indicated; Bottom panel, immunostaining for FUNDC1 in given groups as indicated. Scale bar, 20 μm. (H) Representative transmission electron microscope images showed mitochondrial damage in the hearts of mice in given groups. The yellow arrows indicated injured mitochondria. Scale bar, 300 nm. (I) Western blot analyses showed the expressions of protein, including p-Drp1, Drp-1, Fis1, Mfn2, and OPA1 in indicated groups. (J–M) Quantitative determination of p-Drp1, Drp-1, Fis1, Mfn2, and OPA1 in (I). (N) Western blot analyses showed the expressions of protein, including α-actin, β-MHC in indicated groups. (O,P) Quantitative determination of α-actin, β-MHC in (N). (Q) The heart weight of mice in each group was standardized by body weight. (R) Hematoxylin and eosin (H&E) staining of heart sections from the indicated mice revealed the cross-sectional area of the myocytes. (S) Quantitative determination of the cross-sectional area of cardiomyocytes in (R). *P < 0.05 versus the controls; #P < 0.05 versus homocysteine stimulation alone (n = 6).
