Fig. 7.

Tsg101 promotes autophagic flux in the heart. (A) Representative immunoblots and (B) quantification analysis showing the expression levels of Tsg101 and LC3A/B-II in WT- and TG-hearts. *, p < 0.05 vs. WTs, n = 4. (C) Representative immunoblots and (D/E) quantification analysis showing the protein levels of Tsg101, LC3A/B-II and Keap1 in WT- and TG-mouse hearts treated with or without chloroquine (CQ, 50 mg/kg) for 6 h *, p < 0.05, n = 4. (F) Representative images and (G) quantitative analysis of neonatal rat cardiomyocytes (NRCMs) transfected with the mRFP-GFP-LC3 reporter plasmid and treated with either DMSO (0.001%) or Bafilomycin A1 (BafA1, 100 nM, 4 h). *, p < 0.05, n = 3 litters of neonatal Sprague Dawley rats (1–3 days old) and a total of 20–30 cells per group. Those yellow dots represent combined signals of GFP with mRFP in autophagosomes, whereas those red dots (indicated as arrows in merged images) that do not overlap with GFP fluorescence signal stand for autolysosomes. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)