View : 26 Download: 0

Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice

Title
Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice
Authors
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
이서구강상원오구택이미니
SCOPUS Author ID
이서구scopusscopus; 강상원scopus; 오구택scopus; 이미니scopusscopus
Issue Date
2011
Journal Title
Circulation Research
ISSN
0009-7330JCR Link
Citation
vol. 109, no. 7, pp. 739 - 749
Indexed
SCI; SCIE; SCOPUS WOS scopus
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. © 2011 American Heart Association, Inc.
DOI
10.1161/CIRCRESAHA.111.245530
Appears in Collections:
일반대학원 > 생명·약학부 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE