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. Author manuscript; available in PMC: 2012 Oct 3.
Published in final edited form as: Mol Pharm. 2011 Jul 18;8(5):1709–1719. doi: 10.1021/mp200078n

Figure 1.

Figure 1

Potential mechanisms as to how mitochondrial membrane potential (MMP) could be disrupted during PEI transfection (inhibitors of normal mitochondrial function are shown in boxes on the diagram). PEI could potentially interact with the electron transport chain or F0F1-ATPase, whose contributions to MMP can be observed using rotenone or oligomycin, respectively. The mitochondrial membrane permeability transition pore is formed during times of intracellular stress by the complexation of several proteins, including voltage-dependent anion channel (VDAC), adenine nucleotide translocase (ANT), and cyclophilin D. Cyclosporine a (CsA) is able to prevent the pore from opening and save the cell from apoptosis in certain cases. Additionally, PEI polyplexes could be directly permeabilizing the outer mitochondrial membrane, resulting in a loss of mitochondrial function.