Differential expression patterns of Nqo1, AKR1B8 and Ho-1 in the liver and small intestine of C57BL/6 mice treated with sulforaphane

Luo, Lin; Chen, Yeru; Wu, Deqi; Shou, Jiafeng; Wang, Shengcun; Ye, Jie; Tang, Xiuwen; Wang, Xiu Jun

doi:10.1016/j.dib.2015.09.029

Cited by 14 publications

(6 citation statements)

References 5 publications

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“…Actin antibody (Cat#: R1207) and IgG antibody (Cat#: HA1011) were purchased from Hua-an (Hangzhou, Zhejiang, China). Antibodies against NQO1, HO-1 or AKR1B10 were raised in this laboratory and described previously [37, 38].…”

Section: Methodsmentioning

confidence: 99%

Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer

Wang

Liu

Chi

et al. 2019

Aging

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Alterations in KEAP1/ NF-E2 p45-related factor 2 (NFE2L2/Nrf2) signaling pathway have been reported in 23% lung adenocarcinoma patients, suggesting that deregulation of the pathway is a major cancer driver. Here we report that mitogen-activated protein (MAP) kinase phosphatase 1 (MKP-1) drives tumor growth and drug resistance by up regulating transcription factor Nrf2. In non-small cell lung cancer (NSCLC) cells and xenografts, MKP-1 knockdown triggered the down-regulation of the metabolic enzymes and cytoprotective proteins, which are the target genes of Nrf2. Consequently, the cell growth was markedly inhibited with decrease of tumor metabolisms and GSH contents. Moreover, MKP-1 silencing sensitized NSCLC cells to cisplatin treatment. Mechanistically, MKP-1 inhibited the ubiquitylation of Nrf2 via a direct interaction with the transcription factor. Nrf2 was hence stabilized and its transcriptional program was activated. Notably, Nrf2 elevated MKP-1 expression at transcriptional level. In human lung adenoma tumor samples, high levels of expression of MKP-1, Nrf2, and its target gene heme oxygenase 1 were closely correlated. Thus, MKP-1 and Nrf2 form a forward feedback loop in lung cancer cells, which stabilizing and activating Nrf2 to promote anabolic metabolism and GSH biosynthesis. This study uncovers a novel role of MKP-1 in the malignant evolution of cancers.

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Section: Methodsmentioning

confidence: 99%

Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer

Wang

Liu

Chi

et al. 2019

Aging

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“…Oxidative stress is thought to contribute to the pathogenesis of neurodegenerative diseases, therefore enzymes and transporters with anti-oxidant properties can protect the brain from this fate. Nqo1 is an important enzyme in the detoxification pathways of reactive quinones and reduces oxidative stress (Hwang et al, 2015; Luo et al, 2015; Merrell et al, 2008). Ho-1 catalyzes the rate limiting step in heme catabolism and is also widely accepted as being cytoprotective against several stressors, including electrophiles through the production of bilirubin, a powerful antioxidant and Mrp4 substrate (Luo et al, 2015; Merrell et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Gender-specific expression of ATP-binding cassette ( Abc ) transporters and cytoprotective genes in mouse choroid plexus

2017

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The choroid plexus (CP) and blood-brain barrier (BBB) control the movement of several drugs and endogenous compounds between the brain and systemic circulation. The multidrug resistance associated protein (Mrp) efflux transporters form part of these barriers. Several Mrp transporters are positively regulated by the transcription factor nuclear factor erythroid-2-related factor (Nrf2) in liver. The Mrps, Nrf2 and Nrf2-dependent genes are cytoprotective and our aim was to examine basal gender differences in expression of Mrp transporters, Nrf2 and Nrf2-dependent genes (Nqo1 and Ho-1) in the brain-barriers. Previous studies have shown higher expression of Mrp1, Mrp2 and Mrp4 in female mouse liver and kidney. We hypothesized that similar renal/hepatic gender-specific patterns are present in the brain-barrier epithelia interfaces. qPCR and immunoblot analyses showed that Mrp4, Ho-1 and Nqo1 expression was higher in female CP. Mrp1, Mrp2 and Nrf2 expression in the CP had no gender pattern. Female Mrp1, Mrp2 and Mrp4 mouse brain expressions in remaining brain areas, excluding CP, were higher than male. Functional analysis of Mrp4 in CP revealed active accumulation of the Mrp4 model substrate fluo-cAMP. WT female CP had 10-fold higher accumulation in the vascular spaces than males and 60% higher than Mrp4−/− females. Probenecid blocked all transport. Methotrexate did as well except in Mrp4−/− females where it had no effect, suggesting compensatory induction of transport occurred in Mrp4−/−. Collectively, our findings indicate significant gender differences in expression of Mrp transporters and cytoprotective genes in the CP and BBB.

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“…Gstm1 (glutathione S-transferase mu 1) and aldo-keto-reductase 1C (AKR1C) antisera were kindly provided by Professor John Hayes (University of Dundee, Scotland). Anti-NQO1, anti-AKR1B8, and anti-HO-1 were generated in our laboratory as described previously [39, 40]. DSS (36–50 kD) was from MP Biomedicals (Aurora, OH, USA).…”

Section: Methodsmentioning

confidence: 99%

Synthetic Imine Resveratrol Analog 2-Methoxyl-3,6-Dihydroxyl-IRA Ameliorates Colitis by Activating Protective Nrf2 Pathway and Inhibiting NLRP3 Expression

Chen

Zheng

et al. 2019

Oxidative Medicine and Cellular Longevity

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Resveratrol (RSV) is a naturally occurring polyphenol that exhibits pleiotropic health benefits, including anticolitis and colon cancer-protective activity. Recently, we identified the novel imine RSV analog (IRA), 2-methoxyl-3,6-dihydroxyl-IRA 3,4,5,4-tetramethoxystilbene (C33), as a putative activator of nuclear factor erythroid 2-related factor 2 (Nrf2). The present study was designed to evaluate the ability of C33 to activate the Nrf2 signaling pathway and its anticolitis effect in comparison to RSV. The anticolitis action of C33 was assessed in a mouse model of colitis induced by dextran sulfate sodium (DSS). The effect of C33 on the Nrf2 signaling pathway was examined in vitro and in vivo. Compared to RSV, C33 triggered a more dramatic increase in the expression of genes downstream of Nrf2 in LS174T cells as well as in the small intestine and colon of wild-type (WT) mice. Correlated with its superior ability to activate the cytoprotective Nrf2 pathway, C33 was significantly better in ameliorating DSS-induced colitis by improving the inflammation score, as well as downregulating the markers of inflammation in WT mice. Moreover, induction of the NOD-like receptors family pyrin domain containing 3 (NLRP3) inflammasome by colitis was also significantly inhibited by the IRA. Nrf2 knockout completely abolished the effects of C33, indicating that Nrf2 is the important mechanistic target of C33 in vivo. In conclusion, the novel IRA, C33, has stronger anticolitis effects than RSV. Further studies are warranted to evaluate C33 as a potential therapeutic agent for inflammatory bowel disease and cancer chemoprevention.

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Differential expression patterns of Nqo1, AKR1B8 and Ho-1 in the liver and small intestine of C57BL/6 mice treated with sulforaphane

Cited by 14 publications

References 5 publications

Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer

Interplay of MKP-1 and Nrf2 drives tumor growth and drug resistance in non-small cell lung cancer

Gender-specific expression of ATP-binding cassette ( Abc ) transporters and cytoprotective genes in mouse choroid plexus

Synthetic Imine Resveratrol Analog 2-Methoxyl-3,6-Dihydroxyl-IRA Ameliorates Colitis by Activating Protective Nrf2 Pathway and Inhibiting NLRP3 Expression

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