Fig. 3: Rnd3 overexpression mitigated Dox-induced mitochondrial dysfunction. | Cell Death & Disease

Fig. 3: Rnd3 overexpression mitigated Dox-induced mitochondrial dysfunction.

From: Rnd3 protects against doxorubicin-induced cardiotoxicity through inhibition of PANoptosis in a Rock1/Drp1/mitochondrial fission-dependent manner

Fig. 3

A Representative transmission electron microscope images show the damaged mitochondrial with loss of cristae in cardiomyocytes, scale bar = 10 μm. B, C Quantitative analysis of mitochondrial number per field and mean mitochondrial size (n = 5). D Representative confocal images of Mitochondrial Tracker Red in PBS or Dox-treated cardiomyocytes with Ad-Control or Ad-Rnd3, scale bar = 10 μm. E Quantitative analysis of mitochondrial morphology (n = 5). F Representative confocal microscopic images of JC-1 staining. Red fluorescence represents JC-1 aggregate and green fluorescence denotes JC-1 monomer, scale bar = 10 μm. G Quantitative analysis of the MMP assessed through JC-1 red/green fluorescence intensity (n = 5). H Representative immunofluorescence images of Mito-SOX staining, scale bar = 10 μm. I Quantitative analysis of mitochondria-derived superoxide production in cardiomyocytes (n = 5). J Representative Western blot images of mitochondrial dynamics-related proteins including Drp1-p616 and Drp1 in cardiomyocytes from Ad-Control or Ad-Rnd3 group. K Quantitative analysis of Drp1-p616/Drp1 protein expression (n = 5). Data were presented as mean ± SD. One-way ANOVA was used for statistical analysis in (B), (C), (E), (G), (I), and (K).

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