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. 2020 Sep 14;10(24):11244–11263. doi: 10.7150/thno.46883

Figure 3.

Figure 3

TBC1D15 activates cardiomyocyte mitophagy flux suppressed by hypoxia. A-B. Decrease of autophagosomes and increase of autolysosomes following 9-h hypoxia were attenuated by TBC1D15 overexpression (n = 12-15). Representative images of mRFP-GFP-LC3 transfection (Scale bar = 10 µm) are shown; C-D. Increase of mito-Keima fluorescence intensity ratio (550 nm/440 nm) following 9-h hypoxia was alleviated by TBC1D15 overexpression (n = 10). Representative images of mito-Keima transfection (Scale bar = 5 µm) are displayed. Rectangles denote magnified views. Mean ± SEM, * p < 0.05 vs. Normoxia-LacZ group; # p < 0.05 vs. Hypoxia-LacZ group; E-F. Hypoxia (9 h)-induced suppression of mito-LC3II elevation (normalized to VDAC) in response to bafilomycin A1 (Baf) was ameliorated by TBC1D15 overexpression in NMCMs (n = 6). Bafilomycin A1 was administrated at 100 nM for 2 h. Mean ± SEM, * p < 0.05 vs. corresponding group without Bafilomycin A1; # p < 0.05 vs. Normoxia-LacZ-Baf group; † p < 0.05 vs. Hypoxia-LacZ-Baf group.