Peroxiredoxin I deficiency attenuates phagocytic capacity of macrophage in clearance of the red blood cells damaged by oxidative stress
2012
Han, Y.H., Aging Research Center, KRIBB, Daejeon, Republic of Korea | Kwon, T.H., Aging Research Center, KRIBB, Daejeon, Republic of Korea | Kim, S.U., Aging Research Center, KRIBB, Daejeon, Republic of Korea | Ha, H.L., Aging Research Center, KRIBB, Daejeon, Republic of Korea | Lee, T.H., Aging Research Center, KRIBB, Daejeon, Republic of Korea | Kim, J.M., Chungnam National University, Daejeon, Republic of Korea | Jo, E.K., Chungnam National University, Daejeon, Republic of Korea | Kim, B.Y., Korea Research Institute of Bioscience and Biotechnology, Cheongwon, Republic of Korea | Yoon, D.Y., Konkuk University, Seoul, Republic of Korea | Yu, D.Y., Aging Research Center, KRIBB, Daejeon, Republic of Korea
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∨-/- 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 Pi, I in phagocytosis of macrophage.
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