Aging Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Biochem Biophys Res Commun. 2012 Jul 20;424(1):189-95. doi: 10.1016/j.bbrc.2012.06.113. Epub 2012 Jun 27.
Erythroid cells are highly prone to oxidative damage generated during erythropoiesis and thus are well equipped with antioxidant defense systems. However, their roles have been poorly characterized. Here, we investigated the role of peroxiredoxin II in mouse erythropoiesis. Loss of Prx II significantly increased apoptosis and cell cycle arrest leading to abnormal erythropoiesis at 3 weeks of age when erythropoietin levels were almost same between wild type and Prx II(-/-). In Prx II(-/-) bone marrow cells, DNA tail length as an indicator of the oxidative damage was greatly increased and mRNAs of the molecules associated with DNA damage and repair and transcription regulators of antioxidant enzymes were also significantly increased. In addition, N-Acetyl-L-Cysteine treatment significantly decreased immature erythroblasts and apoptotic cells increased in Prx II(-/-) BMCs. These results strongly demonstrate that Prx II plays an essential role in maintaining normal erythropoiesis by protecting DNA damage.
红细胞在红细胞生成过程中极易产生氧化损伤，因此它们配备了完善的抗氧化防御系统。然而，它们的作用尚未得到充分的描述。在这里，我们研究了过氧化物酶 II 在小鼠红细胞生成中的作用。Prx II 的缺失显著增加了细胞凋亡和细胞周期阻滞，导致在红细胞生成素水平在野生型和 Prx II(-/-) 之间几乎相同的情况下，3 周龄时出现异常的红细胞生成。在 Prx II(-/-) 骨髓细胞中，作为氧化损伤指标的 DNA 尾部长度大大增加，与 DNA 损伤和修复以及抗氧化酶转录调节剂相关的分子的 mRNA 也显著增加。此外，N-乙酰-L-半胱氨酸处理显著减少了 Prx II(-/-)BMC 中幼稚红细胞的数量，并减少了凋亡细胞的增加。这些结果强烈表明，Prx II 通过保护 DNA 损伤在维持正常红细胞生成中发挥着重要作用。
