SIRT2 is a negative regulator of anoxia–reoxygenation tolerance via regulation of 14-3-3 ζ and BAD in H9c2 cells
Abstract
Knockdown or inhibition of SIRT2 enhances biological stress-tolerance. We extend this phenotype showing that SIRT2 knockdown reduces anoxia–reoxygenation injury in H9c2 cells. Gene array analysis following SIRT2 siRNA knockdown identifies 14-3-3 ζ as the most robustly induced gene. SIRT2 knockdown evokes induction of this chaperone, facilitating cytosolic sequestration of BAD with a corresponding reduction in mitochondrial BAD localization. Concurrent siRNA against SIRT2 and 14-3-3 ζ abolishes the SIRT2-depleted cytoprotective phenotype. SIRT2 functions to moderate cellular stress-tolerance, in part, by modulating the levels of 14-3-3 ζ with the concordant control of BAD subcellular localization.
Keywords: SIRT2, BAD, 14-3-3 ζ, H9c2 cells, Anoxia–reoxygenation
To access this article, please choose from the options below
PII: S0014-5793(08)00596-6
doi:10.1016/j.febslet.2008.07.016
© 2008 Federation of European Biochemical Societies. Published by Elsevier BV. All rights reserved.
