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

doi:10.1016/j.bbrc.2012.06.113

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

Department of Life Science

Research output: Contribution to journal › Article › peer-review

14 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 language	English
Pages (from-to)	189-195
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	424
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2012.06.113
State	Published - 20 Jul 2012

Bibliographical note

Funding Information:
This work was supported by the World Class Institute (WCI) Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology of Korea (MEST), by the Grant from the National Research Foundation of Korea ( 0020877 ), the Ministry of Education, Science and Technology, Republic of Korea , and by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MEST) (No. 2011-0030134) and by the KRIBB Research Initiative Program Grant ( KGM2140712 ) in Korea. Do Young Yoon was supported by a Korea Research Foundation (2010-0019306) in Korea. We thanks Dr. Cynthia Dunbar in NHLBI/NIH, MD, U.S.A for technical assistance with experiment of Colony-forming assays.

Keywords

Apoptosis
Cell cycle arrest
DNA damage
Erythropoiesis
Knockout mouse
Peroxiredoxin II

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10.1016/j.bbrc.2012.06.113

Cite this

@article{50c5c978ab1741578f5ad691d9658508,

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

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.",

keywords = "Apoptosis, Cell cycle arrest, DNA damage, Erythropoiesis, Knockout mouse, Peroxiredoxin II",

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

note = "Funding Information: This work was supported by the World Class Institute (WCI) Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology of Korea (MEST), by the Grant from the National Research Foundation of Korea ( 0020877 ), the Ministry of Education, Science and Technology, Republic of Korea , and by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MEST) (No. 2011-0030134) and by the KRIBB Research Initiative Program Grant ( KGM2140712 ) in Korea. Do Young Yoon was supported by a Korea Research Foundation (2010-0019306) in Korea. We thanks Dr. Cynthia Dunbar in NHLBI/NIH, MD, U.S.A for technical assistance with experiment of Colony-forming assays. ",

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T1 - Reactive oxygen species mediated DNA damage is essential for abnormal erythropoiesis in peroxiredoxin II -/- mice

AU - Kwon, Tae Ho

AU - Han, Ying Hao

AU - Hong, So Gun

AU - Lee, Doo Jae

AU - Ha, Hye Lin

AU - Kang, Sang Won

AU - Li, Wei

AU - Yoon, Do Young

AU - Yu, Dae Yeul

N1 - Funding Information: This work was supported by the World Class Institute (WCI) Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology of Korea (MEST), by the Grant from the National Research Foundation of Korea ( 0020877 ), the Ministry of Education, Science and Technology, Republic of Korea , and by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MEST) (No. 2011-0030134) and by the KRIBB Research Initiative Program Grant ( KGM2140712 ) in Korea. Do Young Yoon was supported by a Korea Research Foundation (2010-0019306) in Korea. We thanks Dr. Cynthia Dunbar in NHLBI/NIH, MD, U.S.A for technical assistance with experiment of Colony-forming assays.

PY - 2012/7/20

Y1 - 2012/7/20

N2 - 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.

AB - 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.

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