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

Figure 4.

Figure 4

Inhibition of autophagy flux abolishes TBC1D15 protective effects on cardiomyocytes. NMCMs were transfected with LacZ or TBC1D15 adenovirus in the absence or presence of 9-h hypoxia. Bafilomycin A1 (Baf) was administrated at 100 nM for 2 h. A-B. Hypoxia-induced mitochondrial membrane potential (MMP) loss was attenuated by TBC1D15 overexpression, the effect of which was canceled by Baf (n = 10). Representative images of JC-1 staining (Scale bar = 10 µm) are shown; C-D. Hypoxia-induced cardiomyocyte reactive oxygen species (ROS) accumulation was alleviated by TBC1D15 overexpression, the effect of which was abolished by Baf (n = 10). Representative images of DCFH-DA staining (Scale bar = 10 µm) are displayed; E-F. Hypoxia-induced cardiomyocyte apoptosis was ameliorated by TBC1D15 overexpression, the effect of which was nullified by Baf (n = 12). Representative images of TUNEL/DAPI staining (Scale bar = 25 µm) are exhibited. The white arrows indicate TUNEL positive nuclei. Mean ± SEM, * p < 0.05 vs. Normoxia-LacZ group; # p < 0.05 vs. Hypoxia-LacZ group; † p < 0.05 vs. Hypoxia-TBC1D15 group.