Thioredoxin is associated with endotoxin tolerance in mice

Sano, Haruhiko; Sata, Takeyoshi; Nanri, Hiroki; Ikeda, Masaharu; Shigematsu, Akio

doi:10.1097/00003246-200201000-00027

Cited by 23 publications

(16 citation statements)

References 28 publications

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“…The first study showed that the induction of glutamate cysteine ligase may be an important adaptive response of the alveolar epithelium when under attack by oxidative stress and by lipid peroxidation products such as 4-hydroxy-2-nonenal [91]. A second study has shown that another antioxidant, the thioredoxin gene, is induced by 4-hydroxy-2-nonenal in response to LPS challenge in mice, thereby providing endotoxin tolerance [92].…”

Section: S-glutathiolation Modulation Of Transcription Factorsmentioning

confidence: 99%

Oxidative stress and redox regulation of lung inflammation in COPD

Rahman

Adcock²

2006

Eur Respir J

783

599

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Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (cJun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kBmediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kB-a kinase or the enhanced recruitment and activation of transcriptional coactivators. Enhanced NF-kB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression.Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity.The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/ quercetin and reserveratol), specific spin traps, such as a-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells.Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.

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Section: S-glutathiolation Modulation Of Transcription Factorsmentioning

confidence: 99%

Oxidative stress and redox regulation of lung inflammation in COPD

Rahman

Adcock²

2006

Eur Respir J

783

599

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“…The second Grx (Grx2) gene, which was reported recently, encodes two proteins as a result of alteration of RNA splicing. One of the Grx2 isoforms is located in the mitochondria and the other in the nucleus (54,55). Similar to Trx, Grx also functions in catalyzing thiol/disulfide exchange (57).…”

Section: Dasmentioning

confidence: 99%

“…For example, oxidative stress can easily induce the expression of Trx1 (17,51). A recent study showed that pretreatment of mice with a sublethal dose of lipopolysaccharides increased Trx concentrations that played an important role in the development of endotoxin tolerance via inhibition of ROS (55).…”

Section: Introductionmentioning

confidence: 99%

Thioredoxin Regulation of Ischemic Preconditioning

Das

2004

Antioxidants & Redox Signaling

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Thioredoxins are a class of small redox-regulating proteins that appear to play a crucial role in many oxidative stress-inducible degenerative diseases. A recent study demonstrated a reduction of thioredoxin-1 (Trx1) protein in the ischemic reperfused myocardium. When the same heart was adapted to ischemic stress by preconditioning with repeated cyclic episodes of small duration of ischemia and reperfusion, there was an increased induction of Trx1 expression. Inhibition of Trx1 expression resulted in reduced postischemic ventricular recovery and increased myocardial infarct size in the preconditioned heart. Corroborating these findings, transgenic mouse hearts overexpressing Trx1 were resistant to ischemic reperfusion injury as compared with the hearts from wild-type mice. Thus, it appears that thioredoxin plays a crucial role in cardioprotection induced by preconditioning.

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“…TSA and thioredoxin, two main antioxidant proteins, are likely to be important not only in general cell protection, but also in the promotion of infection and invasion by these pathogenic organisms through protecting against oxidative attack by activated host phagocytic cells [33][34][35]. Following a burn, there is an enormous production of reactive oxygen species (ROS), which is harmful and implicated in inflammation, infection, sepsis, tissue damage, and multiple organ failure [36].…”

Section: Discussionmentioning

confidence: 99%