Figure 7.

Stabilizing Mfn2 conformation prevents giant fusion formation and improves mitophagy coupling in HF myocytes. (A) Representative images showing mCherry-Parkin accumulation and LC3-GFP-mediated autophagosome formation in aged myocytes treated with 1 μM of either TAT-MP1^Gly (left) or TAT-MP2^Gly (right) peptides. (B) Representative images showing mCherry-Parkin accumulation and LC3-GFP-mediated autophagosome formation in HF myocytes treated with 1 μM of either TAT-MP1^Gly (left) or TAT-MP2^Gly (right) peptides. (C) Cell treatment TAT-MP1^Gly (MP1) increased Parkin puncta accumulation in aged myocytes and HF cardiomyocytes, while 1 μM TAT-MP2^Gly (MP2) decreased mCherry-Parkin puncta accumulation in both aged and HF myocytes. β-OHB did not increase the percentage of cells with Parkin-rich areas in cells treated with MP1. (D) Cell treatment TAT-MP1^Gly (MP1) did not affect LC3-mediated autophagosome formation in aged myocytes but increased it HF cardiomyocytes. Cell treatment with 1 μM TAT-MP2^Gly (MP2) decreased mCherry-Parkin puncta accumulation in both aged and HF myocytes. Data expressed as mean ± SEM. n = number of cells from three different animals per each group. *p < 0.05 reflects a significance in HF rabbits vs. aged rabbits; #p < 0.05 reflects a significance in peptide-treated cells vs. corresponding untreated groups.