Fig. 7
- ID
- ZDB-FIG-250725-26
- Publication
- Deng et al., 2025 - Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects
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The knockdown of GREM1 promoted mitochondrial oxidative respiration in AC16 cells. A The knockdown efficiency of GREM1-siRNA interference for 24 h at different concentration in AC16 cells. B The ultrastructure of mitochondria in AC16 cells transfected with 30 nM siRNA for 24 h (n = 3). C–D Mitochondrial potential detected through JC-1 staining (n = 3). Red fluorescence indicates JC-1 aggregates, green fluorescence indicates JC-1 monomers. The ratio of red to green indicates the mitochondrial membrane potential. E–F Mitochondrial ROS stained by MitoSOX Red (n = 3). G The proportion of mito- and glyco- ATP production rate and the ATP production rate from glycolysis respiration, mitochondrial respiration and total respiration in AC16 cells transfected for 24 h, respectively (n = 15). NC: negative control siRNA. *, P < 0.05; ****, P < 0.0001 vs NC |