Author: ["Christopher D. Ferris","Samie R. Jaffrey","Akira Sawa","Masaaki Takahashi","Stephen D. Brady","Roxanne K. Barrow","Steven A. Tysoe","Herman Wolosker","David E. Barañano","Sylvain Doré","Kenneth D. Poss","Solomon H. Snyder"]
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Abstract
Haem oxygenase-1 (HO1) is a heat-shock protein that is induced by stressful stimuli. Here we demonstrate a cytoprotective role for HO1: cell death produced by serum deprivation, staurosporine or etoposide is markedly accentuated in cells from mice with a targeted deletion of the HO1 gene, and greatly reduced in cells that overexpress HO1. Iron efflux from cells is augmented by HO1 transfection and reduced in HO1-deficient fibroblasts. Iron accumulation in HO1-deficient cells explains their death: iron chelators protect HO1-deficient fibroblasts from cell death. Thus, cytoprotection by HO1 is attributable to its augmentation of iron efflux, reflecting a role for HO1 in modulating intracellular iron levels and regulating cell viability.Cite this article
Ferris, C., Jaffrey, S., Sawa, A. et al. Haem oxygenase-1 prevents cell death by regulating cellular iron. Nat Cell Biol 1, 152–157 (1999). https://doi.org/10.1038/11072 