Quercetin Induces the Expression of Peroxiredoxins 3 and 5 via the Nrf2/NRF1 Transcription Pathway

Miyamoto, Naoya; Izumi, Hiroto; Miyamoto, Rie; Kondo, Hiroyuki; Tawara, Akihiko; Sasaguri, Yasuyuki; Kohno, Kimitoshi

doi:10.1167/iovs.10-5777

Cited by 88 publications

(50 citation statements)

References 62 publications

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“…Thus, the SH level in the current study might correspond mainly to the total glutathione level, but that remains to be clarified. Previous studies have reported the possible involvement of thioredoxin system dysregulation in the pathogenesis of glaucoma [41], [42], [51]–[53]; thus, measurement of the thioredoxin level separately from the other thiol groups should be done in the future.…”

Section: Discussionmentioning

confidence: 99%

Status of Systemic Oxidative Stresses in Patients with Primary Open-Angle Glaucoma and Pseudoexfoliation Syndrome

et al. 2012

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BackgroundThe involvement of local and systemic oxidative stress in intraocular pressure (IOP) elevation and optic nerve damage has been hypothesized in the pathogenesis of glaucoma. To test this, we measured the systemic levels of prooxidants and antioxidants by analyzing the blood biochemistry in patients with glaucoma.MethodsPeripheral blood samples were collected from Japanese patients with primary open-angle glaucoma (PG) (n = 206), exfoliation syndrome (EX) (n = 199), and controls (n = 126). Plasma levels of lipid peroxides, ferric-reducing activity, and thiol antioxidant activity were measured by diacron reactive oxygen metabolites (dROM), biological antioxidant potential (BAP), and sulfhydryl (SH) tests, respectively, using a free radical analyzer.ResultsIn the PG, EX, and control groups, the mean ± standard deviation values were 355±63, 357±69, and 348±56 (U. Carr), respectively, for dROM; 1,951±282, 1,969±252, and 2,033±252 (µmol/L), respectively, for BAP (µmol/L); and 614±98, 584±91, and 617±99 (µmol/L), respectively, for SH. The differences in the BAP values were significant between the PG and control groups (p = 0.0062), for SH between the EX and control groups (p = 0.0017), and for SH between the PG and EX groups (p = 0.0026). After adjustment for differences in age and sex among groups using multiple regression analysis, lower BAP values were correlated significantly with PG (p = 0.0155) and EX (p = 0.0049). Higher dROM values with and without glaucoma were correlated with female gender, and lower SH values with older age. There were no significant differences between the higher (≥21 mmHg) and lower (<21 mmHg) baseline IOPs in the PG group or between the presence or absence of glaucoma in the EX group.ConclusionsLower systemic antioxidant capacity that measured by ferric-reducing activity is involved in the pathogenesis of PG and EX.

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Section: Discussionmentioning

confidence: 99%

Status of Systemic Oxidative Stresses in Patients with Primary Open-Angle Glaucoma and Pseudoexfoliation Syndrome

et al. 2012

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“…Nrf1 small interfering RNA (siRNA) has been previously published as Nrf1#1 (37) and was obtained as Stealth RNA interference (RNAi) (Invitrogen). Stealth RNAi negative control (Invitrogen) served as siControl.…”

Section: Methodsmentioning

confidence: 99%

Polo-like kinase 4 transcription is activated via CRE and NRF1 elements, repressed by DREAM through CDE/CHR sites and deregulated by HPV E7 protein

Fischer

Quaas

Wintsche

et al. 2013

Nucleic Acids Research

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Infection by oncogenic viruses is a frequent cause for tumor formation as observed in cervical cancer. Viral oncoproteins cause inactivation of p53 function and false transcriptional regulation of central cell cycle genes. Here we analyze the regulation of Plk4, serving as an example of many cell cycle- and p53-regulated genes. Cell cycle genes are often repressed via CDE and CHR elements in their promoters and activated by NF-Y binding to CCAAT-boxes. In contrast, general activation of Plk4 depends on NRF1 and CRE sites. Bioinformatic analyses imply that NRF1 and CRE are central elements of the transcriptional network controlling cell cycle genes. We identify CDE and CHR sites in the Plk4 promoter, which are necessary for binding of the DREAM (DP, RB-like, E2F4 and MuvB) complex and for mediating repression in G0/G1. When cells progress to G2 and mitosis, DREAM is replaced by the MMB (Myb-MuvB) complex that only requires the CHR element for binding. Plk4 expression is downregulated by the p53-p21WAF1/CIP1-DREAM signaling pathway through the CDE and CHR sites. Cell cycle- and p53-dependent repression is abrogated by HPV E7 oncoprotein. Together with genome-wide analyses our results imply that many cell cycle genes upregulated in tumors by viral infection are bound by DREAM through CDE/CHR sites.

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“…Then, p-Nrf2 translocates into the nucleus, dimerizes with Maf, and binds to AREs in the promoters of the genes that encodes proteins involved in iron homeostasis (heme oxygenase 1 (HO-1) and Ferritin), redox regulation (catalase, peroxiredoxin (Prx), sulfiredoxin (Srx), thioredoxin (Trx), and SOD), and glutathione synthesis (glutathione S -transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione cysteine ligase regulatory subunit (GCLC), glutathione cysteine ligase modulatory subunit (GCLM), and glutathione synthetase, γ-glutamyl cysteine sythetase (γ-GCS)), quinone recycling (NAD(P)H:quinoneoxidoreductase 1 (NQO1)) [109,110]. p-Nrf2 also up-regulates the expression of the genes involved in mitochondrial biogenesis such as mitochondrial transcription factors (e.g., mitochondrial transcriptional factor A (TFAM), Nrf1) [111,112]. …”

Section: Key Neuronal Defense Systemsmentioning

confidence: 99%

Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer’s Disease?

Murphy

Park

2017

IJMS

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Alzheimer’s disease (AD) is a multifaceted disease that is hard to treat by single-modal treatment. AD starts with amyloid peptides, mitochondrial dysfunction, and oxidative stress and later is accompanied with chronic endoplasmic reticulum (ER) stress and autophagy dysfunction, resulting in more complicated pathogenesis. Currently, few treatments can modify the complicated pathogenic progress of AD. Compared to the treatment with exogenous antioxidants, the activation of global antioxidant defense system via Nrf2 looks more promising in attenuating oxidative stress in AD brains. Accompanying the activation of the Nrf2-mediated antioxidant defense system that reduce the AD-causative factor, oxidative stress, it is also necessary to activate the neurotrophic signaling pathway that replaces damaged organelles and molecules with new ones. Thus, the dual actions to activate both the Nrf2 antioxidant system and neurotrophic signaling pathway are expected to provide a better strategy to modify AD pathogenesis. Here, we review the current understanding of AD pathogenesis and neuronal defense systems and discuss a possible way to co-activate the Nrf2 antioxidant system and neurotrophic signaling pathway with the hope of helping to find a better strategy to slow AD.

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Quercetin Induces the Expression of Peroxiredoxins 3 and 5 via the Nrf2/NRF1 Transcription Pathway

Abstract: Quercetin upregulates the antioxidant peroxiredoxins through the activation of the Nrf2/NRF1 transcription pathway and protects against oxidative stress-induced ocular disease.

Cited by 88 publications

References 62 publications

Status of Systemic Oxidative Stresses in Patients with Primary Open-Angle Glaucoma and Pseudoexfoliation Syndrome

Status of Systemic Oxidative Stresses in Patients with Primary Open-Angle Glaucoma and Pseudoexfoliation Syndrome

Polo-like kinase 4 transcription is activated via CRE and NRF1 elements, repressed by DREAM through CDE/CHR sites and deregulated by HPV E7 protein

Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer’s Disease?

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