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Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice
- Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice
- Park J.-G.; Yoo J.-Y.; Jeong S.-J.; Choi J.-H.; Lee M.-R.; Lee M.-N.; Hwa Lee J.; Kim H.C.; Jo H.; Yu D.-Y.; Kang S.W.; Rhee S.G.; Lee M.-H.; Oh G.T.
- Ewha Authors
- 이서구; 강상원; 오구택; 이미니
- SCOPUS Author ID
- 이서구; 강상원; 오구택; 이미니
- Issue Date
- Journal Title
- Circulation Research
- vol. 109, no. 7, pp. 739 - 749
- SCI; SCIE; SCOPUS
- Rationale: Peroxiredoxin 2 (Prdx2), a thiol-specific peroxidase, has been reported to regulate proinflammatory responses, vascular remodeling, and global oxidative stress. Objective: Although Prdx2 has been proposed to retard atherosclerosis development, no direct evidence and mechanisms have been reported. Methods and Results: We show that Prdx2 is highly expressed in endothelial and immune cells in atherosclerotic lesions and blocked the increase of endogenous H2O2 by atherogenic stimulation. Deficiency of Prdx2 in apolipoprotein E-deficient (ApoE-/-) mice accelerated plaque formation with enhanced activation of p65, c-Jun, JNKs, and p38 mitogen-activated protein kinase; and these proatherogenic effects of Prdx2 deficiency were rescued by administration of the antioxidant ebselen. In bone marrow transplantation experiments, we found that Prdx2 has a major role in inhibiting atherogenic responses in both vascular and immune cells. Prdx2 deficiency resulted in increased expression of vascular adhesion molecule-1, intercellular adhesion molecule-1, and monocyte chemotactic protein-1, which led to increased immune cell adhesion and infiltration into the aortic intima. Compared with deficiency of glutathione peroxidase 1 or catalase, Prdx2 deficiency showed a severe predisposition to develop atherosclerosis. Conclusions: Prdx2 is a specific peroxidase that inhibits atherogenic responses in vascular and inflammatory cells, and specific activation of Prdx2 may be an effective means of antiatherogenic therapy. © 2011 American Heart Association, Inc.
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