TCB Publications - Abstract

Meiying Yang, Jie Sun, David F Stowe, Emad Tajkhorshid, Wai-Meng Kwok, and Amadou KS Camara. Knockout of VDAC1 in H9c2 cells promotes oxidative stress-induced cell apoptosis through decreased mitochondrial hexokinase II binding and enhanced glycolytic stress. Cellular Physiology & Biochemistry, 54:853-874, 2020. Published.

YANG2020-ET The role of VDAC1, the most abundant mitochondrial outer membrane protein, in cell death depends on cell types and stimuli. Both silencing and upregulation of VDAC1 in various type of cancer cell lines can stimulate apoptosis. In contrast, in mouse embryonic stem (MES) cells and mouse embryonic fibroblasts (MEFs), the roles of VDAC1 knockout (VDAC1^-/-) in apoptotic cell death are contradictory. The contribution and underlying mechanism of VDAC1^-/- 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.

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