4-Hydroxy-2-Nonenal Enhances Fibronectin Production by IMR-90 Human Lung Fibroblasts Partly via Activation of Epidermal Growth Factor Receptor-Linked Extracellular Signal-Regulated Kinase p44/42 Pathway

Tsukagoshi, Hideo; Kawata, Takefumi; Shimizu, Yūji; Ishizuka, Tamotsu; Dobashi, Kunio; Mori, Masatomo

doi:10.1006/taap.2002.9514

Cited by 28 publications

(14 citation statements)

References 32 publications

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“…Products of lipid peroxidation, such as MDA and unsaturated aldehydes, are capable of inactivating many cellular proteins by forming protein cross-linkages 110–112. 4-Hydroxy-2-nonenal causes depletion of intracellular GSH and induces of peroxide production,113,114 activates epidermal growth factor receptor,115 and induces fibronectin production 116. Lipid peroxidation products, such as isoprostanes and thiobarbituric acid reactive substances, have been used as indirect biomarkers of oxidative stress, and increased levels were shown in the exhaled breath condensate or bronchoalveolar lavage fluid or lung of chronic obstructive pulmonary disease patients or smokers 117–119…”

Section: The Effect Of Oxidative Stress: Genetic Physiological and mentioning

confidence: 99%

Oxidative Stress and Antioxidant Defense

Birben

Şahiner

Saçkesen

et al. 2012

World Allergy Organization Journal

3,846

2,621

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Reactive oxygen species (ROS) are produced by living organisms as a result of normal cellular metabolism and environmental factors, such as air pollutants or cigarette smoke. ROS are highly reactive molecules and can damage cell structures such as carbohydrates, nucleic acids, lipids, and proteins and alter their functions. The shift in the balance between oxidants and antioxidants in favor of oxidants is termed “oxidative stress.” Regulation of reducing and oxidizing (redox) state is critical for cell viability, activation, proliferation, and organ function. Aerobic organisms have integrated antioxidant systems, which include enzymatic and nonenzymatic antioxidants that are usually effective in blocking harmful effects of ROS. However, in pathological conditions, the antioxidant systems can be overwhelmed. Oxidative stress contributes to many pathological conditions and diseases, including cancer, neurological disorders, atherosclerosis, hypertension, ischemia/perfusion, diabetes, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. In this review, we summarize the cellular oxidant and antioxidant systems and discuss the cellular effects and mechanisms of the oxidative stress.

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Section: The Effect Of Oxidative Stress: Genetic Physiological and mentioning

confidence: 99%

Oxidative Stress and Antioxidant Defense

Birben

Şahiner

Saçkesen

et al. 2012

World Allergy Organization Journal

3,846

2,621

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“…In vitro treatment of cells with HNE can cause lipid peroxidation20 and may potentiate oxidative stress through a depletion of intracellular glutathione and induction of peroxide production 21. HNE may also play a role in airway remodeling through activation of the epidermal growth factor receptor22 and induction of fibronectin production 23. Additionally, HNE-protein adducts have been found in the lungs of mice and humans after O 3 exposure 24,25.…”

Section: Mechanisms Of Oxidant-induced Toxicitymentioning

confidence: 99%

“…For example, inhibition of c-Jun NH 2 terminal kinase (JNK) in mice attenuated O 3 -induced inflammation and hyper-responsiveness 52. Additionally, end products of lipid peroxidation activate extracellular signal-regulated kinase p44/42 (Erk1/2), JNK, and p38MAPK and activation can be blocked by NAC 21,23. Activation of these kinases was also accompanied by increased DNA binding activity of the transcription factor activator protein-1 (AP-1), which can lead to the transcription of stress response genes including phase II enzymes (Fig 1).…”

Section: Mechanisms Of Oxidant-induced Toxicitymentioning

confidence: 99%

Oxidants and the pathogenesis of lung diseases

Ciencewicki

Trivedi

Kleeberger

2008

Journal of Allergy and Clinical Immunology

351

280

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The increasing number of population-based and epidemiological associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid (ELF) of the lung. Furthermore, it is clear that inter-individual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (e.g. asthma, COPD, and ARDS), and the potential risk factors (e.g. age, genetics) for enhanced susceptibility to oxidant-induced disease.

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“…Jurkat cells Down regulation of Akt kinase [52] Neurons NGF withdrawal-induced neuronal apoptosis [53] Chlamydia pneumoniae Inhibition of IKK/I kappa B-mediated signaling [54] HBE1 cells Induction of glutamate cysteine ligase through JNK [55] Human lung fibroblasts Activation of epidermal growth factor receptor-linked extracellular signal kinase p44/42 pathway [56] Retinal pigment epithelial cells Induction of vascular endothelial growth factor [57] Macrophages Activation of PKC beta isoforms [58] K562 cells Role in adaptive response of cells to heat and oxidative stress [7] Vascular smooth muscle cells Prevents NO production [59] Vascular smooth muscle cells NF-kappaB activation and formation of isoprostane [60] PC12 cells Activation of JNK pathway [61] Neurons Inhibits constitutive and inducible activity of NF-Kappa B [62] Hepatic stellate cells Reduces tyrosine phosphorylation [63] Human epidermoid carcinoma A431 cells…”

Section: Model System Observed Effect(s); Ref Given In Parenthesesmentioning

confidence: 99%

Self-regulatory role of 4-hydroxynonenal in signaling for stress-induced programmed cell death

Awasthi

Sharma

et al. 2008

Free Radical Biology and Medicine

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Within the last two decades, 4-hydroxynonenal has emerged as an important second messenger involved in the regulation of various cellular processes. Our recent studies suggest that HNE can induce apoptosis in various cells through the death receptor Fas (CD95)-mediated extrinsic pathway as well as through the p53-dependent intrinsic pathway. Interestingly, through its interaction with the nuclear protein Daxx, HNE can self-limit its apoptotic role by translocating Daxx to cytoplasm where it binds to Fas and inhibits Fas-mediated apoptosis. In this paper, after briefly describing recent studies on various biological activities of HNE, based on its interactions with Fas, Daxx, and p53, we speculate on possible mechanisms through which HNE may affect a multitude of cellular processes and draw a parallel between signaling roles of H 2 O 2 and HNE.

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4-Hydroxy-2-Nonenal Enhances Fibronectin Production by IMR-90 Human Lung Fibroblasts Partly via Activation of Epidermal Growth Factor Receptor-Linked Extracellular Signal-Regulated Kinase p44/42 Pathway

Cited by 28 publications

References 32 publications

Oxidative Stress and Antioxidant Defense

Oxidative Stress and Antioxidant Defense

Oxidants and the pathogenesis of lung diseases

Self-regulatory role of 4-hydroxynonenal in signaling for stress-induced programmed cell death

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