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Figure 6 | Molecular Neurodegeneration

Figure 6

From: Regulation of mitochondrial permeability transition pore by PINK1

Figure 6

Blockade of mPTP opening by CsA attenuates the respiratory defect in PINK1 −/− MEFs. A. Representative oxygraphs of PINK1−/− and +/+ MEFs energized with glucose (10 mM) in the presence of CsA (1 μM). The arrows indicate the time MEFs are added to the chamber. B. Oxygen consumption, which represents the endogenous respiratory activity in PINK1−/− and +/+ MEFs after treatment with CsA (1 μM). C. Representative oxygraphs of PINK1−/− and +/+ MEFs energized with 10 mM glutamate/malate (complex I substrate), 10 mM succinate (complex II substrate) or 1 mM TMPD/1 mM ascorbate (complex IV substrate) in the presence of CsA (1 μM). Arrows indicate the time of the addition of either the substrate or oligomycin (2 μM). D. Graph showing State 3 respiratory activity for complex I, complex II and complex IV in PINK1−/− and +/+ MEFs permeabilized with digitonin after treatment with CsA (1 μM). E. Representative oxygraphs of PINK1−/− and +/+ MEFs energized with 10 mM glutamate/malate (complex I substrate), 10 mM succinate (complex II substrate) or 1 mM TMPD/1 mM ascorbate (complex IV substrate) after treatment with FK-506 (5 μM). Arrows indicate the time of the addition of either the substrate or oligomycin (2 μM). F. Graph showing State 3 respiratory activity for complex I, complex II and complex IV in PINK1−/− and +/+ MEFs permeabilized with digitonin after treatment with FK-506 (5 μM). All data are expressed as mean ± SEM. * p < 0.05.

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