Age-Related Macular Degeneration (AMD) Transmitochondrial Cybrids Protected from Cellular Damage and Death by Human Retinal Progenitor Cells (hRPCs)

Figure 3

AMD cybrids cocultured with hRPCs show decreased expression levels of apoptosis, autophagy, ER stress, and antioxidant genes at 48 hr. In order to examine the role of hRPCs in protecting AMD cybrids from mtDNA-mediated cellular damage, we used qRT-PCR analyses to measure the differential gene expression profiles of apoptosis, autophagy, ER stress, and antioxidant genes in AMD cybrids with hRPCs versus AMD cybrids without hRPCs. (a–d) In AMD cybrids, hRPCs significantly downregulated apoptosis genes (a): BAX (, ), CASP3 (, ), CASP7 (, ), and CASP9 (, ); autophagy genes (b): ATG5 (, ), ATG12 (, ), LAMP2 (, ), LC3B (, ), and PARK2 (, ); ER stress genes (c): DDIT3 (, ), and XBP1 (, ); and antioxidant genes (d): GPX (, ), SOD2 (, ), and NQO1 (, ) compared to untreated AMD cybrids. Data are represented as , normalized to the control, which is normal cybrids assigned a value of 1 (dotted line). Data between the treatment and control groups were analyzed for differences by performing one-sample -tests on the expression fold change values from the five cybrid lines for each gene (), comparing the values with a hypothetical value of 1.

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