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. 2015 Jul 31;24(21):2561–2576. doi: 10.1089/scd.2015.0066

FIG. 2.

FIG. 2.

Deficiency of Cisd2 in miPSCs results in the inhibition of the mitochondrial potential. (A) TEM analysis of the ultrastructure of the Cisd2+/+ and Cisd2−/− miPSCs. Arrows indicate the mitochondria. (B) Pie plot showing the summary of mitochondria gene in Cisd2−/− miPSCs, including mitochondrial localization, fission and fusion, inner membrane translocation, outer membrane translocation, mitochondrial protein import, and membrane polarization and potential. Cisd2 deficiency impairs the ability to sustain the mitochondrial potential. (C) Mitochondria potential of different passage Cisd2+/+, Cisd2+/−, and Cisd2−/− fibroblasts (p1, p3, and p5) and miPSCs (p10, p20, and p30) were determined with JC-1 assay. (D) Western blots of mitochondria permeability protein in Cisd2+/+, Cisd2+/−, and Cisd2−/− miPSCs. Expression of Cisd2 protein maintains Hax1, Bnip3, and Sod1 expression. α-Tubulin was used as a loading control. (E) Quantitative RT-PCR analysis of the mitochondrial potential-associated genes in Cisd2+/+, Cisd2+/−, and Cisd2−/− miPSCs. Data represent mean ± SD in independent experiment. *P < 0.05.