Redox Regulation of Lipopolysaccharide-mediated Sulfiredoxin Induction, Which Depends on Both AP-1 and Nrf2

Kim, Hojin; Jung, Yoon Young; Shin, Bong Soo; Kim, Hyeryeon; Song, Hyunsook; Bae, Soo Han; Rhee, Sue Goo; Jeong, Woojin

doi:10.1074/jbc.m110.126839

Cited by 54 publications

(47 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 16 addition, an AP-1 like-sequence was found embedded within the more distal ARE motifs. This specific structural feature has been previously described by other groups (Inamdar et al, 1996;Kim et al, 2010). These findings suggest a putative involvement of this specific DNA region in the regulation of CRYAB expression under conditions of redox imbalance in muscle cells.…”

Section: Discussionmentioning

confidence: 54%

“…Moreover, as previously described for other Nrf2 target genes (Inamdar et al, 1996;Kim et al, 2010), an activator protein-1 (AP-1)-like sequence (TCAGTCA) was found embedded within the most distal ARE motif (Fig. 4A).…”

Section: Transcriptional Start Site (Tss)mentioning

confidence: 77%

“…myoblasts MAPK signalling pathways are known to be involved in the up-regulation and activation of c-Jun and Nrf2 transcription factors (Kim et al, 2010;Elsby et al, 2003;Rubio et al, 2013). .…”

Section: Inhibition Of Jnk Activity Rescues the Cryab Basal Levels Ofmentioning

confidence: 99%

See 2 more Smart Citations

Alpha B-crystallin induction in skeletal muscle cells under redox imbalance is mediated by a JNK-dependent regulatory mechanism

Fittipaldi

Neri

Dimauro

et al. 2015

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 54%

Section: Transcriptional Start Site (Tss)mentioning

confidence: 77%

See 1 more Smart Citation

Alpha B-crystallin induction in skeletal muscle cells under redox imbalance is mediated by a JNK-dependent regulatory mechanism

Fittipaldi

Neri

Dimauro

et al. 2015

Free Radical Biology and Medicine

View full text Add to dashboard Cite

“…However, oxidation of cysteines in KEAP1 relieves binding and allows Nrf2 to accumulate, enter the nucleus and exert its activity (Zhang and Hannink, 2003;Zhang et al, 2004;Yamamoto et al, 2008). It therefore also follows that inherent to M1 activation and increased NOX2 activity, there is a certain level of Nrf2 activation and induction of antioxidant proteins (Kim et al, 2010;Kong et al, 2010), which again opposes NF-kB activity (Kong et al, 2010;Cuadrado et al, 2014) and oxidant levels to uphold redox homeostasis. Although timing is crucial, there is a broad assumption that acquisition of the M2 phenotype is beneficial in acute or chronic brain disease (Cherry et al, 2014;Hu et al, 2015).…”

mentioning

confidence: 99%

Microglia antioxidant systems and redox signalling

Vilhardt¹,

Haslund-vinding

Jaquet³

et al. 2016

British J Pharmacology

105

View full text Add to dashboard Cite

For many years, microglia, the resident CNS macrophages, have been considered only in the context of pathology, but microglia are also glial cells with important physiological functions. Microglia-derived oxidant production by NADPH oxidase (NOX2) is implicated in many CNS disorders. Oxidants do not stand alone, however, and are not always pernicious. We discuss in general terms, and where available in microglia, GSH synthesis and relation to cystine import and glutamate export, and the thioredoxin system as the most important antioxidative defence mechanism, and further, we discuss in the context of protein thiolation of target redox proteins the necessity for tightly localized, timed and confined oxidant production to work in concert with antioxidant proteins to promote redox signalling. NOX2-mediated redox signalling modulates the acquisition of the classical or alternative microglia activation phenotypes by regulating major transcriptional programs mediated through NF-κB and Nrf2, major regulators of the inflammatory and antioxidant response respectively. As both antioxidants and NOX-derived oxidants are co-secreted, in some instances redox signalling may extend to neighboring cells through modification of surface or cytosolic target proteins. We consider a role for microglia NOX-derived oxidants in paracrine modification of synaptic function through long term depression and in the communication with the adaptive immune system. There is little doubt that a continued foray into the functions of the antioxidant response in microglia will reveal antioxidant proteins as dynamic players in redox signalling, which in concert with NOX-derived oxidants fulfil important roles in the autocrine or paracrine regulation of essential enzymes or transcriptional programs. LINKED ARTICLESThis article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc Abbreviations Aβ, amyloid-β peptide 1-42; DAMP, damage-associated molecular pattern molecules; GCL, glutamate cysteine ligase; GPx, GSH peroxidase; HNE, 4-hydroxy-2-nonenal; HO-1, haem oxygenase-1; KEAP1, Kelch-like ECH-associated protein; LTD, long-term depression; PLA 2 , phospholipase A 2 ; Prx, peroxiredoxins; Trx, thioredoxin; TrxR, thioredoxin reductase; xCT, cystine-glutamate exchanger IntroductionMicroglia, the resident immune cells of the brain, are exquisitely sensitive cells, which through a large and unique repertoire of sensing cell surface receptors (Hickman et al., 2013) responding to ligands of exogenous or endogenous nature (Kettenmann et al., 2013) continuously survey the brain parenchyma for even the smallest deviation from homeostasis. When the fine, motile processes of microglia encounter a problem, microglia assume an activation phenotype adapted to the quick resolution of damage and return to homeostasis. If instigating insults cannot be resolved, chronic microglia activation ensues. The differing nature of...

show abstract

“…Nrf2 regulates immune responses by inducing antioxidant and phase II detoxifying enzymes, thereby demonstrating an anti-inflammatory role also [46]. Nrf2 is normally present in the cytoplasm bound to Kelch-like ECH-associated protein-1 (Keap1).…”

Section: Redox Modulation Of Inflammatory Pathways-nrf2 and Nfjb In Imentioning

confidence: 99%

Multi-target drugs to address multiple checkpoints in complex inflammatory pathologies: evolutionary cues for novel “first-in-class” anti-inflammatory drug candidates: a reviewer’s perspective

Mathew

Unnikrishnan

2015

Inflamm. Res.

View full text Add to dashboard Cite

Inflammation is a complex, metabolically expensive process involving multiple signaling pathways and regulatory mechanisms which have evolved over evolutionary timescale. Addressing multiple targets of inflammation holistically, in moderation, is probably a more evolutionarily viable strategy, as compared to current therapy which addresses drug targets in isolation. Polypharmacology, addressing multiple targets, is commonly used in complex ailments, suggesting the superior safety and efficacy profile of multi-target (MT) drugs. Phenotypic drug discovery, which generated successful MT and first-in-class drugs in the past, is now re-emerging. A multi-pronged approach, which modulates the evolutionarily conserved, robust and pervasive cellular mechanisms of tissue repair, with AMPK at the helm, regulating the complex metabolic/immune/redox pathways underlying inflammation, is perhaps a more viable strategy than addressing single targets in isolation. Molecules that modulate multiple molecular mechanisms of inflammation in moderation (modulating TH cells toward the anti-inflammatory phenotype, activating AMPK, stimulating Nrf2 and inhibiting NFκB) might serve as a model for a novel Darwinian "first-in-class" therapeutic category that holistically addresses immune, redox and metabolic processes associated with inflammatory repair. Such a multimodal biological activity is supported by the fact that several non-calorific pleiotropic natural products with anti-inflammatory action have been incorporated into diet (chiefly guided by the adaptive development of olfacto-gustatory preferences over evolutionary timescales) rendering such molecules, endowed with evolutionarily privileged molecular scaffolds, naturally oriented toward multiple targets.

show abstract

Redox Regulation of Lipopolysaccharide-mediated Sulfiredoxin Induction, Which Depends on Both AP-1 and Nrf2

Cited by 54 publications

References 81 publications

Alpha B-crystallin induction in skeletal muscle cells under redox imbalance is mediated by a JNK-dependent regulatory mechanism

Alpha B-crystallin induction in skeletal muscle cells under redox imbalance is mediated by a JNK-dependent regulatory mechanism

Microglia antioxidant systems and redox signalling

Multi-target drugs to address multiple checkpoints in complex inflammatory pathologies: evolutionary cues for novel “first-in-class” anti-inflammatory drug candidates: a reviewer’s perspective

Contact Info

Product

Resources

About