Reactive oxygen species mediated DNA damage is essential for abnormal erythropoiesis in peroxiredoxin II -/- mice

Tae Ho Kwon, Ying Hao Han, So Gun Hong, Doo Jae Lee, Hye Lin Ha, Sang Won Kang, Wei Li, Do Young Yoon, Dae Yeul Yu

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

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 3weeks 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.

Original languageEnglish
Pages (from-to)189-195
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume424
Issue number1
DOIs
StatePublished - 20 Jul 2012

Keywords

  • Apoptosis
  • Cell cycle arrest
  • DNA damage
  • Erythropoiesis
  • Knockout mouse
  • Peroxiredoxin II

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