FEBS Letters · 2010 · 225 citations · 27 references
Life SciencesAgricultural BiotechnologyMolecular BiologyApoptosisBioenergeticsMitochondrial BiologyHeat Stress ToleranceMitochondrial BioenergeticsMitochondrial FunctionMitochondrial PhysiologyMitochondrial Stress ResponsesCell Death AssaysCell Viability AssaysCell Viability PreservationCytochrome C Release BlockadeHeat Shock Protein RegulationHeat Treatment EffectsReactive Oxygen Species Generation
In this study, we identified and functionally characterized the mitochondrial heat shock protein 70 (mtHsp70). Over-expression of mtHsp70 suppressed heat- and H(2)O(2)-induced programmed cell death (PCD) in rice protoplasts, as reflected by higher cell viability, decreased DNA laddering and chromatin condensation. Mitochondrial membrane potential (Δψ(m)) after heat shock was destroyed gradually in protoplasts, but mtHsp70 over-expression showed higher Δψ(m) relative to the vector control cells, and partially inhibited cytochrome c release from mitochondria to cytosol. Heat treatment also significantly increased reactive oxygen species (ROS) generation, a phenomenon not observed in protoplasts over-expressing mtHsp70. Together, these results suggest that mtHsp70 may suppress PCD in rice protoplasts by maintaining mitochondrial Δψ(m) and inhibiting the amplification of ROS.
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The expanding role of mitochondria in apoptosis.
Negative regulation of the Apaf-1 apoptosome by Hsp70
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