Peroxiredoxin 5 regulates adipogenesis-attenuating oxidative stress in obese mouse models induced by a high-fat diet

Kim, Mi Hye; Park, Sun-Ji; Kim, Jung‐Hak; Seong, Jung Bae; Kim, Kyung–Min; Woo, Hyun Ae; Lee, Dong Seok

doi:10.1016/j.freeradbiomed.2018.05.061

Cited by 41 publications

(44 citation statements)

References 51 publications

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“…Future studies using these new models, as well as complete knockout mouse models, will help us better understand the physiological roles of PRDXs and provide possible therapeutic targets for drugs against diseases, such as cancer and inflammatory and metabolic diseases. [94,96] High-fat diet Fat, liver…”

Section: Discussionmentioning

confidence: 99%

“…The Prdx5 gene is located on mouse chromosome 19 and there are four alternative forms of Prdx5 protein-coding transcripts [31]. A Prdx5-knockout mouse line has been generated by the homologous recombination approach [94]. Another Prdx5-knockout mouse line that is generated by the gene trap approach is commercially available [95].…”

Section: Genetics and Knockout Mouse Strainsmentioning

confidence: 99%

“…Prdx5 deficiency leads to increased susceptibility to high-fat-diet-induced obesity, and thus Prdx5-knockout mice fed a high-fat diet show several metabolic abnormalities, including increased body weight, adipocyte hypertrophy, fat accumulation in the liver, hepatic steatosis, and an increased triglyceride level in the serum [94,96].…”

Section: Metabolismmentioning

confidence: 99%

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Knockout Mouse Models for Peroxiredoxins

Lee

2020

Antioxidants

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Peroxiredoxins (PRDXs) are members of a highly conserved peroxidase family and maintain intracellular reactive oxygen species (ROS) homeostasis. The family members are expressed in most organisms and involved in various biological processes, such as cellular protection against ROS, inflammation, carcinogenesis, atherosclerosis, heart diseases, and metabolism. In mammals, six PRDX members have been identified and are subdivided into three subfamilies: typical 2-Cys (PRDX1, PRDX2, PRDX3, and PRDX4), atypical 2-Cys (PRDX5), and 1-Cys (PRDX6) subfamilies. Knockout mouse models of PRDXs have been developed to investigate their in vivo roles. This review presents an overview of the knockout mouse models of PRDXs with emphases on the biological and physiological changes of these model mice.

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Section: Discussionmentioning

confidence: 99%

Section: Genetics and Knockout Mouse Strainsmentioning

confidence: 99%

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Knockout Mouse Models for Peroxiredoxins

Lee

2020

Antioxidants

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“…Notably, since Prx5 is located within the cytosol and the mitochondria, it can effectively remove intracellular ROS (15). Previous studies have determined that Prx5 is a potent antioxidant enzyme that contributes to cellular homeostasis by scavenging intracellular ROS (16)(17)(18)(19). However, the role of Prx5 in protection against glutamate-induced neuronal cell death remains unclear.…”

mentioning

confidence: 99%

Peroxiredoxin 5 Inhibits Glutamate-Induced Neuronal Cell Death through the Regulation of Calcineurin-Dependent Mitochondrial Dynamics in HT22 Cells

Kim

Lee

et al. 2019

Molecular and Cellular Biology

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Glutamate is an essential neurotransmitter in the central nervous system (CNS). However, high glutamate concentrations can lead to neurodegenerative diseases. A hallmark of glutamate toxicity is high levels of reactive oxygen species (ROS), which can trigger Ca2+ influx and dynamin-related protein 1 (Drp1)-mediated mitochondrial fission. Peroxiredoxin 5 (Prx5) is a well-known cysteine-dependent peroxidase enzyme. However, the precise effects of Prx5 on glutamate toxicity are still unclear. In this study, we investigated the role of Prx5 in glutamate-induced neuronal cell death. We found that glutamate treatment induces endogenous Prx5 expression and Ca2+/calcineurin-dependent dephosphorylation of Drp1, resulting in mitochondrial fission and neuronal cell death. Our results indicate that Prx5 inhibits glutamate-induced mitochondrial fission through the regulation of Ca2+/calcineurin-dependent dephosphorylation of Drp1, and it does so by scavenging cytosolic and mitochondrial ROS. Therefore, we suggest that Ca2+/calcineurin-dependent mitochondrial dynamics are deeply associated with glutamate-induced neurotoxicity. Consequently, Prx5 may be used as a potential agent for developing therapies against glutamate-induced neurotoxicity and neurodegenerative diseases where it plays a key role.

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“…Multiple functions have been assigned to the human ortholog of Ahp1p from various studies. Some of the important functions of the Prx5 could include down-regulation of the cyclin dependant kinase-5 (Cdk5), clearance of ROS and RNS, protection against oligomeric Aβassociated mitochondrial fragmentation, endoplasmic stress and metal-induced toxicity including iron-induced toxicity represented in Figure 5 [17][18][19][20].…”

Section: Ahp1p and Its Human Ortholog Prx5: Significance In Neuronsmentioning

confidence: 99%

Insights from Yeast on Oxidative Stress in Alzheimer’s Disease, Focusing on Ahp1p/Prx5

Macreadie¹,

Dhakal²

2019

obm geriatr

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The yeast, Saccharomyces cerevisiae, the model eukaryote, has provided much understanding of molecular and cellular biology, as well as insights into many human diseases. In this paper we review how yeast studies are contributing to knowledge about the role of oxidative damage to cell health, and how one of the key players in Alzheimer's disease, amyloid beta (Aβ) is linked to the reactive oxygen species response involving AHP1, which encodes an alkyl hydroperoxidase, Ahp1p, a protein involved in protection from lipid peroxidation.

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Peroxiredoxin 5 regulates adipogenesis-attenuating oxidative stress in obese mouse models induced by a high-fat diet

Cited by 41 publications

References 51 publications

Knockout Mouse Models for Peroxiredoxins

Knockout Mouse Models for Peroxiredoxins

Peroxiredoxin 5 Inhibits Glutamate-Induced Neuronal Cell Death through the Regulation of Calcineurin-Dependent Mitochondrial Dynamics in HT22 Cells

Insights from Yeast on Oxidative Stress in Alzheimer’s Disease, Focusing on Ahp1p/Prx5

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