Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress
Meiying Yang, Jie Sun, David F. Stowe, Emad Tajkhorshid, Wai-Meng Kwok, Amadou K.S. Camara
Abstract
BACKGROUND/AIMS: in oxidative stress-induced cell death in cardiac cells has not been established. We hypothesized that VDAC1 is an essential regulator of oxidative stress-induced cell death in H9c2 cells. METHODS: consumption rate (OCR) and extracellular acidification rate (ECAR) with a Seahorse XFp analyzer. RESULTS: and WT H9c2 cells. CONCLUSION: in H9c2 cells enhances oxidative stress-mediated cell apoptosis that is directly linked to the reduction of mitochondria-bound HKII and concomitantly associated with enhanced ROS production, ECAR, and PPR.
Topics & Concepts
Oxidative stressVDAC1Cell biologyGlycolysisApoptosisHexokinaseMitochondrionChemistryBiochemistryBiologyMetabolismGeneEscherichia coliBacterial outer membraneMitochondrial Function and PathologyATP Synthase and ATPases ResearchCancer, Hypoxia, and Metabolism