Multiple Roles of Peroxiredoxins in Inflammation

Knoops, Bernard; Argyropoulou, Vasiliki; Becker, Sarah; Ferté, Laura; Кузнецова, О. А.

doi:10.14348/molcells.2016.2341

Cited by 121 publications

(56 citation statements)

References 66 publications

(93 reference statements)

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“…In contrast, when the concentration of H 2 O 2 or ONOO − surpasses their signaling threshold, they promote oxidation of biomolecules, such as proteins, lipids, and particularly, nucleic acids [1, 3]. High levels of ROS released under control in phagocytes provide protection from invading bacteria and viruses [4]; however, uncontrolled and high levels of ROS breakdown cellular components leading to cancer, neurological disorders, and cardiovascular disease, to name a few [5–7]. Oxidation of the genome represents a critical location in which oxidatively-derived damage under high levels of ROS can lead to these diseases.…”

Section: Introduction1mentioning

confidence: 99%

Formation and processing of DNA damage substrates for the hNEIL enzymes

Fleming

Burrows

2017

Free Radical Biology and Medicine

112

135

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Reactive oxygen species (ROS) are harnessed by the cell for signaling at the same time as being detrimental to cellular components such as DNA. The genome and transcriptome contain instructions that can alter cellular processes when oxidized. The guanine (G) heterocycle in the nucleotide pool, DNA, or RNA is the base most prone to oxidation. The oxidatively-derived products of G consistently observed in high yields from hydroxyl radical, carbonate radical, or singlet oxygen oxidations under conditions modeling the cellular reducing environment are discussed. The major G base oxidation products are 8-oxo-7,8-dihydroguanine (OG), 5-carboxamido-5-formamido-2-iminohydantoin (2Ih), spiroiminodihydantoin (Sp), and 5-guanidinohydantoin (Gh). The yields of these products show dependency on the oxidant and the reaction context that includes nucleoside, single-stranded DNA (ssDNA), double-stranded DNA (dsDNA), and G-quadruplex DNA (G4-DNA) structures. Upon formation of these products in cells, they are recognized by the DNA glycosylases in the base excision repair (BER) pathway. This review focuses on initiation of BER by the mammalian Nei-like1-3 (NEIL1-3) glycosylases for removal of 2Ih, Sp, and Gh. The unique ability of the human NEILs to initiate removal of the hydantoins in ssDNA, bulge-DNA, bubble-DNA, dsDNA, and G4-DNA is outlined. Additionally, when Gh exists in a G4 DNA found in a gene promoter, NEIL-mediated repair is modulated by the plasticity of the G4-DNA structure provided by additional G-runs flanking the sequence. On the basis of these observations and cellular studies from the literature, the interplay between DNA oxidation and BER to alter gene expression is discussed.

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Section: Introduction1mentioning

confidence: 99%

Formation and processing of DNA damage substrates for the hNEIL enzymes

Fleming

Burrows

2017

Free Radical Biology and Medicine

112

135

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“…Expression of Prx6 in various tissues has been shown to rise in marine animal models following bacterial stimuli (22,23). The same effect has been seen in mouse bone marrow-derived macrophages following stimulation with interferon gamma and lipopolysaccharide (24). One study demonstrated translocation of Prx6 to the plasma membrane during neutrophil activation and that this is required for optimal function of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (25).…”

Section: Discussionmentioning

confidence: 92%

Peroxiredoxin 6 Serum Levels and Risk of Neutropenic Infections in Diffuse Large B-cell Lymphoma

et al. 2019

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Background/Aim: Diffuse large B-cell lymphoma (DLBCL) is an aggressive malignancy where antioxidant enzyme peroxiredoxin 6 (Prx6) has previously been associated with adverse outcomes. Its systemic effects in DLBCL are unknown. Materials and Methods: This study included 53 patients with DLBCL, five patients with primary central nervous system lymphoma (PCNSL) and 20 healthy controls. The expression of Prx6 was evaluated immunohistochemically in DLBCL tissue samples and compared to its expression in blood serum. Results: Prx6 expression was the highest in healthy controls, followed by DLBCL patients and PCNSL patients. Febrile neutropenic infection after the first treatment course was associated with low pre-treatment Prx6 serum levels (<14 ng/ml) (p=0.025, OR=8.615, 95% confidence interval=1.032-71.933). Serum levels of Prx6 recovered after treatment (p=0.006). Conclusion: Patients with low Prx6 levels might be more prone to treatment-related adverse effects through elevated levels of oxidative stress. Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma, accounting for 30-40% of all cases. DLBCL is a group of different diseases that displays considerable variability regarding clinical presentation and prognosis (1). Oxidative stress markers such as 8-hydroxydeoxyguanosine (8-OHdG) and antioxidant enzymes, thioredoxin and glutamate-cysteine ligase seem to have a prognostic relevance in certain types of DLBCL where they are strongly expressed compared to more indolent types of lymphoma (2, 3). Peroxiredoxins (Prxs) are a group of six antioxidant enzymes that reduce hydrogen peroxide. In a recent retrospective immunohistochemical study, strong cytoplasmic intensity of peroxiredoxin 6 (Prx6) in DLBCL was shown to be associated with adverse outcomes in patients, while other Prxs (Prxs 1, 2, 3 and 5) were not associated with disease presentation or prognosis (4). In the present study, we immunohistochemically assessed 8-OHdG and Prx6 expression in tumour tissue samples and compared the results with their expression in patients' serum to explore their systemic effects. In addition, healthy controls and patients with primary central nervous system lymphoma (PCNSL) were included, in order to evaluate differences between CNS lymphoma and systemic disease. Patients and Methods Patients. A total of 58 patients who had diagnostic blood serum samples available were retrospectively selected for the study. Study subjects comprised 53 patients with DLBCL, five patients with PCNSL and 20 healthy controls. Blood levels of Prx6 and 8-OHdG were measured using ELISA in all participants. Patient serum samples were obtained at the time of diagnosis and again at a median of 9 months, with a range of 1-38 months, after the end of treatment (n=24). Routine diagnostic biopsy samples were immunohisto-chemically stained for Prx6 and 8-OHdG. Five patients with DLBCL were lacking a representative biopsy sample. Patients were treated at the Oulu University Hospital in 2003-2017. Clinical data were collected from ...

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“…In addition, PRDX4 has a role in regulating the activation of NF-ĸB transcription factor and TNF-related apoptosis-inducing ligand (TRAIL) [56]. TRAIL is a transmembrane protein involved in apoptosis extrinsic pathway by binding to receptors DR4 or DR5.…”

Section: Peroxiredoxin-4 41 Peroxiredoxin-4 and Its Functionmentioning

confidence: 99%

Silencing of Peroxiredoxin-4 in Anticancer Activity of Gamma-Tocotrienol

Aznan¹,

Jubri²

2020

Synthetic Biology - New Interdisciplinary Science

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Peroxiredoxin-4 (PRDX4) is known to have a role in protecting cells from oxidative stress. It has been previously reported to increase in HepG2 liver cancer cells treated with gamma-tocotrienol (GTT). As GTT treatment potentially kills the cancer cell by regulating multiple signaling pathways, this study aims to determine the involvement of PRDX4 in GTT anticancer activity by silencing the PRDX4 gene. The efficiency of PRDX4 silencing is achieved by optimizing HepG2 cell density, effect of serum presence in transduction media, incubation time of the cells with lentivirus, polybrene concentration, puromycin dose, functional titer, and multiplicity of infection (MOI) of the lentivirus. Silenced HepG2-PRDX4 cells (HepG2-shRNA-PRDX4) were treated with 70 μM of GTT for 48 h. GTT treatment significantly decreased the HepG2-shRNA-PRDX4 cell viability, increased apoptosis rate, and reduced free radical production compared to untreated HepG2-shRNA-PRDX4 cells. These findings are further supported by proteomic analysis, which showed that pro-apoptotic and DNA damage proteins were upregulated, and proteins involved in cell cycle arrest, carcinogenesis, and anti-apoptotic signaling pathways were downregulated in HepG2-shRNA-PRDX4 cells treated with GTT compared to control. In conclusion, PRDX4 plays a role in GTT anticancer activity by increasing free radical production and oxidative damage to induce apoptosis in HepG2 cell.

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Multiple Roles of Peroxiredoxins in Inflammation

Cited by 121 publications

References 66 publications

Formation and processing of DNA damage substrates for the hNEIL enzymes

Formation and processing of DNA damage substrates for the hNEIL enzymes

Peroxiredoxin 6 Serum Levels and Risk of Neutropenic Infections in Diffuse Large B-cell Lymphoma

Silencing of Peroxiredoxin-4 in Anticancer Activity of Gamma-Tocotrienol

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