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http://dx.doi.org/10.5483/BMBRep.2012.45.10.082

Peroxiredoxin I deficiency attenuates phagocytic capacity of macrophage in clearance of the red blood cells damaged by oxidative stress  

Han, Ying-Hao (Aging Research Center)
Kwon, Tae-Ho (Aging Research Center)
Kim, Sun-Uk (Aging Research Center)
Ha, Hye-Lin (Aging Research Center)
Lee, Tae-Hoon (Aging Research Center)
Kim, Jin-Man (Department of Pathology, College of Medicine, Chungnam National University)
Jo, Eun-Kyeong (Department of Microbiology, College of Medicine, Chungnam National University)
Kim, Bo-Yeon (Chemical Biology Research Center and World Class Institute, Korea Research Institute of Bioscience and Biotechnology)
Yoon, Do-Young (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University)
Yu, Dae-Yeul (Aging Research Center)
Publication Information
BMB Reports / v.45, no.10, 2012 , pp. 560-564 More about this Journal
Abstract
The role of peroxiredoxin (Prx) I as an erythrocyte antioxidant defense in red blood cells (RBCs) is controversial. Here we investigated the function of Prx I by using Prx $I^{-/-}$ and Prx I/$II^{-/-}$ mice. Prx $I^{-/-}$ mice exhibited a normal blood profile. However, Prx I/$II^{-/-}$ mice showed more significantly increased Heinz body formation as compared with Prx $II^{-/-}$ mice. The clearance rate of Heinz body-containing RBCs in Prx $I^{-/-}$ mice decreased significantly through the treatment of aniline hydrochloride (AH) compared with wild-type mice. Prx I deficiency decreased the phagocytic capacity of macrophage in clearing Heinz body-containing RBCs. Our data demonstrate that Prx I deficiency did not cause hemolytic anemia, but showed that further increased hemolytic anemia symptoms in Prx $II^{-/-}$ mice by attenuating phagocytic capacity of macrophage in oxidative stress damaged RBCs, suggesting a novel role of Prx I in phagocytosis of macrophage.
Keywords
Heinz body; Hemolytic anemia; Macrophage; Peroxiredoxin; Phagocytosis;
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