Peroxiredoxin 2 Deficiency Exacerbates Atherosclerosis in Apolipoprotein E-Deficient Miceopen access
- Authors
- Park, Jong-Gil; Yoo, Ji-Young; Jeong, Se-Jin; Choi, Jae-Hoon; Lee, Mi-Ran; Lee, Mi-Ni; Lee, Jeong Hwa; Kim, Hyoung Chin; Jo, Hanjoong; Yu, Dae-Yeul; Kang, Sang Won; Rhee, Sue Goo; Lee, Mun-Han; Oh, Goo Taeg
- Issue Date
- Sep-2011
- Publisher
- LIPPINCOTT WILLIAMS & WILKINS
- Keywords
- peroxiredoxin 2; atherosclerosis; inflammation; VCAM-1; ICAM-1
- Citation
- CIRCULATION RESEARCH, v.109, no.7, pp.739 - U80
- Indexed
- SCIE
SCOPUS
- Journal Title
- CIRCULATION RESEARCH
- Volume
- 109
- Number
- 7
- Start Page
- 739
- End Page
- U80
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/167701
- DOI
- 10.1161/CIRCRESAHA.111.245530
- ISSN
- 0009-7330
- Abstract
- 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.
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