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 Blood, 12 November 2009, Vol. 114, No. 20, pp. 4546-4551.
Prepublished online as a Blood First Edition Paper on August 11, 2009; DOI 10.1182/blood-2009-05-224188.

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RED CELLS, IRON, AND ERYTHROPOIESIS

Specific iron chelators determine the route of ferritin degradation

Ivana De Domenico1, Diane McVey Ward2, and Jerry Kaplan2

Departments of 1 Internal Medicine and 2 Pathology, University of Utah School of Medicine, Salt Lake City

Deferoxamine (DFO) is a high-affinity Fe (III) chelator produced by Streptomyces pilosus. DFO is used clinically to remove iron from patients with iron overload disorders. Orally administered DFO cannot be absorbed, and therefore it must be injected. Here we show that DFO induces ferritin degradation in lysosomes through induction of autophagy. DFO-treated cells show cytosolic accumulation of LC3B, a critical protein involved in autophagosomal-lysosomal degradation. Treatment of cells with the oral iron chelators deferriprone and desferasirox did not show accumulation of LC3B, and degradation of ferritin occurred through the proteasome. Incubation of DFO-treated cells with 3-methyladenine, an autophagy inhibitor, resulted in degradation of ferritin by the proteasome. These results indicate that ferritin degradation occurs by 2 routes: a DFO-induced entry of ferritin into lysosomes and a cytosolic route in which iron is extracted from ferritin before degradation by the proteasome.


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Related Article in Blood Online:

Mining ferritin iron: 2 pathways
Elizabeth C. Theil
Blood 2009 114: 4325-4326. [Full Text] [PDF]



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E. C. Theil
Mining ferritin iron: 2 pathways
Blood, November 12, 2009; 114(20): 4325 - 4326.
[Full Text] [PDF]


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