Peroxiredoxin II preserves cognitive function against age-linked hippocampal oxidative damage

Kim, Sun Uk; Jin, Mei; Kim, Yoon Sik; Lee, Sangeun; Cho, Yee Sook; Cho, Kyoung Joo; Lee, Kyu-Sun; Kim, Yang In; Kim, Gyung Whan; Kim, Jin Man; Lee, Tae Hoon; Lee, Young Ho; Shong, Minho; Kim, Hyung Chun; Chang, Kyu Tae; Yu, Dae Yeul; Lee, Dong Seok

doi:10.1016/j.neurobiolaging.2009.05.017

Cited by 53 publications

(38 citation statements)

References 69 publications

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“…The connection between ERK activation and Prx-2 in the hippocampus has been shown previously (85), and we report here that Klotho induces ERK phosphorylation in hippocampal neurons. Using a specific pharmacological ERK inhibitor, U0126, we have shown that the presence of the inhibitor slightly but non-significantly inhibited Klotho-induced induction of Prx-2, suggesting that the ERK-mediated pathway was not critical in the effect of Klotho on neuronal survival.…”

Section: Discussionsupporting

confidence: 87%

The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System

Zeldich

Chen

Colvin

et al. 2014

Journal of Biological Chemistry

190

133

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Background:Klotho is an age suppressor protein whose brain function is unknown. Results: Klotho protects hippocampal neurons from glutamate and amyloid ␤-induced oxidative damage through the induction of the thioredoxin/peroxiredoxin system. Conclusion: Klotho is neuroprotective via the regulation of the redox system. Significance: Understanding the mechanism underlying Klotho-induced neuroprotection may lead to the development of novel therapeutic approaches against neurodegeneration.

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Section: Discussionsupporting

confidence: 87%

The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System

Zeldich

Chen

Colvin

et al. 2014

Journal of Biological Chemistry

190

133

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“…Dietary vitamin E alleviated a number of PRX II deficiencyrelated impairments, including a restoration of the cognitive decline in aged PRX II-deficient mice (218), suggesting that PRX II helps maintain hippocampal synaptic plasticity against age-related oxidative damage. In a differential proteomic analysis, PRX 1 from aged rat temporal cortex tissue is carbonylated, suggesting that this enzyme contributes to the decline in cognitive function that occurs during aging (431).…”

Section: Massaad and Klannmentioning

confidence: 97%

“…PRX has been shown to contribute its antioxidative capability in the realm of aging-and AD-related cognitive dysfunction. Specifically, PRX II-deficient mice were shown to have increased mitochondrial ROS generation and pronounced age-related LTP impairments compared to their wild-type littermates (218). These mice also exhibited an impairment in the activation of synaptic plasticity-related signaling pathways involving CREB, CaMKII, and ERK, indicating that PRX II is necessary for maintaining redox homeostasis (218).…”

Section: Catalasementioning

confidence: 99%

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Massaad

Klann

2011

Antioxidants & Redox Signaling

471

350

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The brain is a metabolically active organ exhibiting high oxygen consumption and robust production of reactive oxygen species (ROS). The large amounts of ROS are kept in check by an elaborate network of antioxidants, which sometimes fail and lead to neuronal oxidative stress. Thus, ROS are typically categorized as neurotoxic molecules and typically exert their detrimental effects via oxidation of essential macromolecules such as enzymes and cytoskeletal proteins. Most importantly, excessive ROS are associated with decreased performance in cognitive function. However, at physiological concentrations, ROS are involved in functional changes necessary for synaptic plasticity and hence, for normal cognitive function. The fine line of role reversal of ROS from good molecules to bad molecules is far from being fully understood. This review focuses on identifying the multiple sources of ROS in the mammalian nervous system and on presenting evidence for the critical and essential role of ROS in synaptic plasticity and memory. The review also shows that the inability to restrain either age-or pathology-related increases in ROS levels leads to opposite, detrimental effects that are involved in impairments in synaptic plasticity and memory function.

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“…Other studies show that Prx 2 overexpression provides resistance to cytotoxic agents [48,49]. Prx 2 is considered to be a marker associated with age-linked oxidative damage [50], but further studies are required to elucidate the mechanisms of MP-induced increased in Prx 2.…”

Section: Gene Expression Level Of Peroxiredoxinmentioning

confidence: 99%

Proteomic analysis of methyl parathion-responsive proteins in Sparus latus liver

Chen

Huang

2011

Fish & Shellfish Immunology

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Peroxiredoxin II preserves cognitive function against age-linked hippocampal oxidative damage

Cited by 53 publications

References 69 publications

The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System

The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System

Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory

Proteomic analysis of methyl parathion-responsive proteins in Sparus latus liver

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