Fig. 7
Effect of internalized mitochondrial function on the regulation of energy metabolism and cell viability in MCF-7 cells. Normal mitochondria (Mito) and dysfunctional mitochondria with the mitochondrial DNA (mtDNA) A8344G mutation (Mito8344) were isolated from normal and myoclonic epilepsy with ragged-red fibres (MERRF) syndrome cybrid cells, respectively. After cells received mitochondrial transplantation with (P-Mito and P-Mito8344) or without Pep-1 modification (Mito and Mito8344) for 3 days, mitochondrial basal respiration and glycolysis were measured by monitoring consumption rates (OCRs) and extracellular acidification rates (ECARs) in real time, respectively (a). Mitochondrial ATP turnover, maximal respiration and reserved capacity were analysed by individually calculating the OCR response to mitochondrial ATP synthase inhibitor Oligomycin (Olygo, 1 μM), an uncoupler of FCCP (0.3 μM) and complex I inhibitor of Rotenone (1 μM). Quantifications of the OCR and ECAR were normalized to the quantity of cells (pmoles/min/protein OD) (a). The profile of metabolic phenotypes according to respiration and glycolysis showed metabolic reprogramming by mitochondrial transplantation (b). The effect of the Mito8344 or P-Mito83344 treatments on cell viability was evaluated by WST-1 proliferation assay on days 1, 3, 5 and 7 (c). * p < 0.05, difference relative to the control (Ctrl) group. # p < 0.05, difference relative to the Pep-1 group. + p < 0.05, difference between the Mito and P-Mito groups