NFκB and AP-1 mediate transcriptional responses to oxidative stress in skeletal muscle cells

Zhou, Lucy Z.-H.; Johnson, Alexandra P; Rando, Thomas A.

doi:10.1016/s0891-5849(01)00719-5

Cited by 282 publications

(196 citation statements)

References 59 publications

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“…This finding shows that the interplay between cell-derived ROS and catalase in tumor cells is a rather dynamic process and not at all static. Based on the findings by Zhou et al (2001), the control of catalase expression by H 2 O 2 might be controlled by redox-sensitive transcription factors like activating protein-1 (AP-1) or nuclear factor κ light-chainenancer of activated B cells (NF-κB). Our findings also allow the speculation that tumor cells in a high antioxidative environment will be protected by this environment against their own apoptosis-inducing ROS signaling pathways, but most likely, they will not express much catalase on their surface due to the missing inducing signal by H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

Extracellular localization of catalase is associated with the transformed state of malignant cells

Böhm¹,

Heinzelmann²,

Motz³

et al. 2015

Biological Chemistry

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Oncogenic transformation is dependent on activated membrane-associated NADPH oxidase (NOX). However, the resultant extracellular superoxide anions are also driving the NO/peroxynitrite and the HOCl pathway, which eliminates NOX-expressing transformed cells through selective apoptosis induction. Tumor progression is dependent on dominant interference with intercellular apoptosis-inducing ROS signaling through membraneassociated catalase, which decomposes H 2 O 2 and peroxynitrite and oxidizes NO. Particularly, the decomposition of extracellular peroxynitrite strictly requires membraneassociated catalase. We utilized small interfering RNA (siRNA)-mediated knockdown of catalase and neutralizing antibodies directed against the enzyme in combination with challenging H 2 O 2 or peroxynitrite to determine activity and localization of catalase in cells from three distinct steps of multistage oncogenesis. Nontransformed cells did not generate extracellular superoxide anions and only showed intracellular catalase activity. Transformed cells showed superoxide anion-dependent intercellular apoptosis-inducing ROS signaling in the presence of suboptimal catalase activity in their membrane. Tumor cells exhibited tight control of intercellular apoptosis-inducing ROS signaling through a high local concentration of membrane-associated catalase. These data demonstrate that translocation of catalase to the outside of the cell membrane is already associated with the transformation step. A strong local increase in the concentration of membrane-associated catalase is achieved during tumor progression and is controlled by tumor cell-derived H 2 O 2 and by transglutaminase.

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Section: Discussionmentioning

confidence: 99%

Extracellular localization of catalase is associated with the transformed state of malignant cells

Böhm¹,

Heinzelmann²,

Motz³

et al. 2015

Biological Chemistry

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“…However, the mechanism by which it stimulates these antioxidant enzymes is unknown. Many evidences have shown that the expressions of all these enzymes genes are directly or indirectly regulated by redox-sensitive transcription factors, such as NF-B and AP-1 [18,19] . Hepatic IPC is associated with activation of NFkappaB [20] , which may account for its stimulation of the endogenous antioxidant enzymes.…”

Section: Discussionmentioning

confidence: 99%

Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Yuan

Ma²,

Gong³

et al. 2005

WJG

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AIM:To investigate effects of ischemic pre-conditioning on the liver endogenous oxidant-antioxidant system during ischemia/reperfusion injury. METHODS:Twenty-four male Sprague-Dawley rats were randomly divided into sham-operated (Sham), ischemia/ reperfusion (I/R), ischemic pre-conditioning plus ischemia/ reperfusion (IPC) groups. Serum ALT, AST and hyaluronic acid levels were assayed and pathologic alterations observed. Liver malondialdehyde (MDA) contents, endogenous antioxidant enzymes, superoxidase dismutase (SOD), catalase (CAT), gultathionine peroxidase (GSH-Px) activities, neutrophils accumulation marker, myeloperoxidase (MPO) activities were measured respectively. RESULTS:Compared with I/R group, sinusoidal endothelial cells as well as hepatocytes damages, as assessed biochemically and histochemically, were improved significantly in IPC group; neutrophils infiltration was also markedly reduced. In IPC group, liver peroxidation, as measured by MDA contents, was significantly decreased when compared with I/R group; endogenous antioxidant enzymes, SOD, CAT and GSH-Px activities were markedly higher than that in I/R group. CONCLUSION:Ischemic pre-conditioning exerts protective effects on both hepatic sinusoidal endothelial cells and hepatocytes during liver I/R injury. Its mechanisms may involve dimunition of neutrophils infiltration and modulation of the imbalance of endogenous oxidant-antioxidant system in the organism.

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“…NF-КB (p50) was studied in this project because of its role in modulation of response to oxidative stress (Beinke et al 2004, Zhou et al 2001.…”

Section: Induction Of Nf-кb In Cells Expressing Ngalmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani

Halabian

Rouhbakhsh

et al. 2010

Cell Stress and Chaperones

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Lipocalin-2 (Lcn2, NGAL) is a member of the lipocalin super family with diverse function such as the induction of apoptosis, the suppression of bacterial growth, and modulation of inflammatory response. Much interest has recently been focused on the physiological/pathological role of the lipocalin-2 that is considered to be a novel protective factor against oxidative stress. However, its precise biological roles in this protection are not fully understood. In this report we intended to test the effect of lipocalin-2 on the expression of heme oxygenase (1, 2) and superoxide dismutase (1, 2) which are two strong antioxidants. NGAL was cloned to pcDNA3.1 plasmid by using genetic engineering method. The recombinant vector was transfected to CHO and HEK293T to establish stable cell expressing NGAL and the expression of HO-1, 2 and SOD 1, 2 were compared with appropriate controls by RT-PCR and western blot. On the other hand, expression of NGAL was suppressed by siRNA transfection in order to study the effect of lipocalin-2 on mentioned genes/proteins. The results showed that the expression of HO-1 and SOD 1, 2 enzymes were higher in cells expressing recombinant lipocalin-2 compared with the control cells. Although the expression of HO-1 was lower in NGAL silencing cells, the expression of SOD 1 and SOD 2 were higher. Our data suggest that NGAL is a potent inducer of HO-1 and somewhat SOD 1 and SOD 2 and it appears that part of antioxidant property of NGAL could be attributed to the induction of HO-1and SOD 1, 2 .

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NFκB and AP-1 mediate transcriptional responses to oxidative stress in skeletal muscle cells

Cited by 282 publications

References 59 publications

Extracellular localization of catalase is associated with the transformed state of malignant cells

Extracellular localization of catalase is associated with the transformed state of malignant cells

Modulation of liver oxidant-antioxidant system by ischemic preconditioning during ischemia/reperfusion injury in rats

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

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