期刊
INTERNATIONAL JOURNAL OF HEMATOLOGY
卷 95, 期 2, 页码 149-159出版社
SPRINGER JAPAN KK
DOI: 10.1007/s12185-011-0988-3
关键词
Iron overload; Iron chelation; Erythroid differentiation; Intracellular reactive oxygen species (ROS); Apoptosis
类别
资金
- Grants-in-Aid for Scientific Research [23591369, 19679004, 22790902] Funding Source: KAKEN
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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