Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice.

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 H(2)O(2) 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 an

SUBMITTER: Park JG 

PROVIDER: S-EPMC5474748 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature