Redox atlas of the mouse

Godoy, José R.; Funke, Maria; Ackermann, Waltraud; Haunhorst, Petra; Oesteritz, Sabrina; Capani, Francisco; Elsässer, Hans Peter; Lillig, Christopher Horst

doi:10.1016/j.bbagen.2010.05.006

Cited by 113 publications

(68 citation statements)

References 85 publications

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“…11 Consistent with this notion, the roles of Prdxl and Prdx2 are also apparent in phenotypes of the corresponding knockout mice, including hemolytic anemia and cellular senescence, 12,13 and differences in tissue distribution. 14 A recent report showed that Prdx2 is more susceptible than Prdx1 to hyperoxidation in cells subjected to sustained global oxidative stress, 15 which suggests that Prdx2 deficiency may lead to accelerated atherosclerosis due to failure to eliminate ROS. However, Prdx2 has not yet been reported to be connected to atherosclerosis.…”

mentioning

confidence: 99%

Peroxiredoxin 2 Deficiency Exacerbates Atherosclerosis in Apolipoprotein E–Deficient Mice

Park

Yoo

Jeong

et al. 2011

Circulation Research

110

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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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mentioning

confidence: 99%

Peroxiredoxin 2 Deficiency Exacerbates Atherosclerosis in Apolipoprotein E–Deficient Mice

Park

Yoo

Jeong

et al. 2011

Circulation Research

110

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“…PRXs are a large antioxidant family with limited literature in relation to AKI. Among them, PRX3 is a unique member because it is exclusively localized in the mitochondria and regulates mitochondrial H 2 O 2 levels22. Two studies reported that PRX3 is up-regulated in experimental renal ischemia-reperfusion injury1718.…”

Section: Discussionmentioning

confidence: 99%

Tubular Peroxiredoxin 3 as a Predictor of Renal Recovery from Acute Tubular Necrosis in Patients with Chronic Kidney Disease

Chang

et al. 2017

Sci Rep

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Peroxiredoxin 3 (PRX3) is a mitochondrial antioxidant that regulates apoptosis in various cancers. However, whether tubular PRX3 predicts recovery of renal function following acute kidney injury (AKI) remains unknown. This retrospective cohort study included 54 hospitalized patients who had AKI with biopsy-proven acute tubular necrosis (ATN). The study endpoint was renal function recovery within 6 months. Of the 54 enrolled patients, 25 (46.3%) had pre-existing chronic kidney disease (CKD) and 33 (61%) recovered renal function. Tubular PRX3 expression was higher in patients with ATN than in those without renal function recovery. The level of tubular but not glomerular PRX3 expression predicted renal function recovery from AKI (AUROC = 0.76). In multivariate Cox regression analysis, high PRX3 expression was independently associated with a higher probability of renal function recovery (adjusted hazard ratio = 8.99; 95% CI 1.13–71.52, P = 0.04). Furthermore, the discriminative ability of the clinical model for AKI recovery was improved by adding tubular PRX3. High tubular PRX3 expression was associated with a higher probability of renal function recovery from ATN. Therefore, tubular PRX3 in combination with conventional predictors can further improve recovery prediction and may help with risk stratification in AKI patients with pre-existing CKD.

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“…It was previously shown that the Grx system has positive impact on insulin secretion [16, 46, 47]. Furthermore, tissue-specific expression of Grx was reported [48]. Plasmatic Grx activity differs between healthy subjects and patients suffering from diabetes mellitus type 2 [49].…”

Section: Discussionmentioning

confidence: 99%

“…The beta-cell is especially prone to oxidative damage for its low expression of enzymes such as catalase and glutathione peroxidase, which are mainly involved in detoxification of H 2 O 2 [29]. The glutaredoxin system has been proven to be expressed in mice islets [48] and may represent an important alternative pathway in detoxification of ROS for the beta-cell. The four mammalian glutaredoxins are located in the major cellular compartments [8, 21, 26, 60] and are thereby involved in a broad range of functions.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity

et al. 2017

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The onset and progression of diabetes mellitus type 2 is highly contingent on the amount of functional beta-cell mass. An underlying cause of beta-cell decay in diabetes is oxidative stress, which markedly affects the insulin producing pancreatic cells due to their poor antioxidant defence capacity. Consequently, disturbances of cellular redox signaling have been implicated to play a major role in beta-cell loss in diabetes mellitus type 2. There is evidence suggesting that the glutaredoxin (Grx) system exerts a protective role for pancreatic islets, but the exact mechanisms have not yet been elucidated. In this study, a mouse model for diabetes mellitus type 2 was used to gain further insight into the significance of Grx for the islets of Langerhans in the diabetic metabolism. We have observed distinct differences in the expression levels of Grx in pancreatic islets between obese, diabetic db mice and lean, non-diabetic controls. This finding is the first report about a decrease of Grx expression levels in pancreatic islets of diabetic mice which was accompanied by declining insulin secretion, increase of reactive oxygen species (ROS) production level, and cell cycle alterations. These data demonstrate the essential role of the Grx system for the beta-cell during metabolic stress which may provide a new target for diabetes mellitus type 2 treatment.

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Redox atlas of the mouse

Cited by 113 publications

References 85 publications

Peroxiredoxin 2 Deficiency Exacerbates Atherosclerosis in Apolipoprotein E–Deficient Mice

Peroxiredoxin 2 Deficiency Exacerbates Atherosclerosis in Apolipoprotein E–Deficient Mice

Tubular Peroxiredoxin 3 as a Predictor of Renal Recovery from Acute Tubular Necrosis in Patients with Chronic Kidney Disease

Differential expression of islet glutaredoxin 1 and 5 with high reactive oxygen species production in a mouse model of diabesity

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