| The effect of iron overload and chelation on erythroid differentiation. | |
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MedLine Citation:
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PMID: 22193844 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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We investigated the mechanisms of hematopoietic disorders caused by iron overload and chelation, in particular, the inhibition of erythroblast differentiation. Murine c-kit(+) progenitor cells or human CD34(+) peripheral blood hematopoietic progenitors were differentiated in vitro to the erythroid lineage with free iron and/or an iron chelator. Under iron overload, formation of erythroid burst-forming unit colonies and differentiation to mature erythroblasts were significantly suppressed; these effects were canceled by iron chelation with deferoxamine (DFO). Moreover, excessive iron burden promoted apoptosis in immature erythroblasts by elevating intracellular reactive oxygen species (ROS). Interestingly, both DFO and a potent anti-oxidant agent reduced intracellular ROS levels and suppressed apoptosis, thus restoring differentiation to mature erythroblasts. Accordingly, intracellular ROS may represent a new therapeutic target in the treatment of iron overload. |
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Authors:
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Kazuki Taoka; Keiki Kumano; Fumihiko Nakamura; Masataka Hosoi; Susumu Goyama; Yoichi Imai; Akira Hangaishi; Mineo Kurokawa |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-12-23 |
Journal Detail:
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Title: International journal of hematology Volume: - ISSN: 1865-3774 ISO Abbreviation: - Publication Date: 2011 Dec |
Date Detail:
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Created Date: 2011-12-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9111627 Medline TA: Int J Hematol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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