Oxidative stress and TNF-a induce histone Acetylation and NF-кB/AP-1 activation in Alveolar epithelial cells: Potential mechanism In gene transcription in lung inflammation

Rahman, Irfan; Gilmour, Peter S.; Jiménez, Luis A.; MacNee, William

doi:10.1007/978-1-4615-1087-1_28

Cited by 174 publications

(176 citation statements)

References 39 publications

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“…Notably in this regard, mild transgenic overexpression of sirt1 in mouse hearts was associated with protection against oxidative stress, and ageing, while high overexpressors displayed enhanced cardiomyopathy [212]. In addition to regulation of the sirtuin class of histone deacetylases by oxidative stress, HDACs linked to transcriptional activities of NF-kB, and AP-1 [213][214][215]) may be inhibited by H 2 O 2 (or environmental stresses), and a role for S-nitrosylation has likewise been identified with HDACs in the context of CREB induced gene expression [216].…”

Section: Redox Regulation Of Transcription Factorsmentioning

confidence: 99%

“…While all these observations provide compelling links between H 2 O 2 , changes in histone acetylation and, enhanced transcriptional activity, some of these studies examined conditions of overt stress, characterized by decreases in levels of GSH, increases in GSSG, and evidence of tyrosine nitration [214,215], and highlight the need for additional studies to understand redox regulation of chromatin remodeling factors under physiological settings, which also should entail identification of target amino acids that are oxidized.…”

Section: Redox Regulation Of Transcription Factorsmentioning

confidence: 99%

See 1 more Smart Citation

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Janssen–Heininger¹,

Mossman²,

Heintz³

et al. 2008

Free Radical Biology and Medicine

705

652

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Section: Redox Regulation Of Transcription Factorsmentioning

confidence: 99%

Section: Redox Regulation Of Transcription Factorsmentioning

confidence: 99%

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Janssen–Heininger¹,

Mossman²,

Heintz³

et al. 2008

Free Radical Biology and Medicine

705

652

View full text Add to dashboard Cite

“…TNF-α has been shown in animal models to induce pathological features associated with COPD, such as an inflammatory cell infiltrate into the lungs, pulmonary fibrosis and emphysema [62,63]. It enhances neutrophil chemotaxis and migration by inducing the expression of chemokine interleukin 8 (IL-8) and upregulating endothelial adhesion molecules [64,65]. In vivo, elevated levels of TNF-α have been demonstrated in peripheral blood, bronchial biopsies, induced sputum and BALF of patients with stable COPD compared with control subjects [66][67][68][69][70].…”

Section: Role Of Tnf-α In Asthma and Copdmentioning

confidence: 99%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

119

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Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation, has been implicated in several inflammatory conditions. It plays a significant role in many inflammatory diseases of lung. Given that there is significant literature supporting the pathobiologic role of TNF-α in asthma, mainly in severe refractory asthma, and COPD, TNF-α inhibitors (infliximab, golimumab and etanercept) are now regarded as potential new medications in asthma and COPD management. The studies reported in literature indicate that TNF-α inhibitors are effective in a relatively small subgroup of patients with severe asthma, possibly defined by an increased TNF axis, but they seem to be ineffective in COPD, although an observational study demonstrated that TNF-α inhibitors were associated with a reduction in the rate of COPD hospitalisation among patients with COPD receiving these agents to treat their rheumatoid arthritis. These findings require a smart approach because there is still good reason to target TNF-α, perhaps in a more carefully selected patient group. TNF-α treatment should therefore not be thrown out, or abandoned. Indeed, since severe asthma and COPD are heterogeneous diseases that have characteristics that occur with different phenotypes remained poorly characterized and little known about the underlying pathobiology contributing to them, it is likely that definition of these phenotypes and choice of the right outcome measure will allow us to understand which kind of patients can benefit from TNF-α inhibitors.

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“…However, this balance is perturbed under pathological conditions, resulting in an overwhelming proinflammatory activity [134]. Among the transcription factors involved in modulating proinflammatory responses, NF-κB is the most important one under hyperoxic conditions, although recent data have also implicated AP-1.…”

Section: Transcription Factors and Proinflammatory Cytokines In Hypermentioning

confidence: 99%

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells☆

Zaher

Miller

Morrow

et al. 2007

Free Radical Biology and Medicine

122

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Mechanical ventilation with hyperoxia is necessary to treat critically ill patients. However, prolonged exposure to hyperoxia leads to the generation of excessive reactive oxygen species (ROS), which can cause acute inflammatory lung injury. One of the major effects of hyperoxia is the injury and death of pulmonary epithelium, which is accompanied by increased levels of pulmonary proinflammatory cytokines and excessive leukocyte infiltration. A thorough understanding of the signaling pathways leading to pulmonary epithelial cell injury/death may provide some insights into the pathogenesis of hyperoxia-induced acute inflammatory lung injury. This review focuses on epithelial responses to hyperoxia and some of the major factors regulating pathways to epithelial cell injury/death, and proinflammatory responses upon exposure to hyperoxia. We discuss in detail some of the most interesting players, such as, NF-κB, that can modulate both proinflammatory responses and cell injury/death of lung epithelial cells. A better appreciation for the functions of these factors will no doubt help us to delineate the pathways to hyperoxic cell death and proinflammatory responses.

show abstract

Oxidative stress and TNF-a induce histone Acetylation and NF-кB/AP-1 activation in Alveolar epithelial cells: Potential mechanism In gene transcription in lung inflammation

Cited by 174 publications

References 39 publications

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

Redox-based regulation of signal transduction: Principles, pitfalls, and promises

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells☆

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