4-hydroxynonenal induces glutamate cysteine ligase through JNK in HBE1 cells

Dickinson, David B.; Iles, Karen E.; Watanabe, Nobuo; Iwamoto, Takeo; Zhang, Hongqiao; Krzywanski, David M.; Forman, Henry Jay

doi:10.1016/s0891-5849(02)00991-7

Cited by 112 publications

(97 citation statements)

References 56 publications

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“…Numerous studies have shown that physiological concentrations of HNE can stimulate cellular proliferation (187)(188)(189), differentiation (190,191), and cytoprotective response (181,(192)(193)(194)(195)(196)(197), through affecting multiple signaling pathways. As low as 0.5 μM, HNE can induce transcription of glutamate cysteine ligase, the first enzyme of GSH synthesis, through activation of the Nrf2-EpRE signaling pathways (198).…”

Section: Signaling Pathways Activated By Hnementioning

confidence: 99%

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

Forman

Fukuto

Miller

et al. 2008

Archives of Biochemistry and Biophysics

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During the past several years, major advances have been made in understanding how reactive oxygen species (ROS) and nitrogen species (RNS) participate in signal transduction. Identification of the specific targets and the chemical reactions involved still remains to be resolved with many of the signaling pathways in which the involvement of reactive species has been determined. Our understanding is that ROS and RNS have second messenger roles. While cysteine residues in the thiolate (ionized) form found in several classes of signaling proteins can be specific targets for reaction with H 2 O 2 and RNS, better understanding of the chemistry, particularly kinetics, suggests that for many signaling events in which ROS and RNS participate, enzymatic catalysis is more likely to be involved than non-enzymatic reaction. Due to increased interest in how oxidation products, particularly lipid peroxidation products, also are involved with signaling, a review of signaling by 4-hydroxy-2-nonenal (HNE) is included. This article focuses on the chemistry of signaling by ROS, RNS, and HNE and will describe reactions with selected target proteins as representatives of the mechanisms rather attempt to comprehensively review the many signaling pathways in which the reactive species are involved. Keywords signaling; glutathione; thioredoxin; oxidants; reactive oxygen species; thiols; peroxide; nitric oxide; peroxynitrite; 4-hydroxynonenal; cysteine; hydrogen peroxide; protein tyrosine phosphatase; reactive nitrogen species; eNOS; iNOS; nNOS; soluble guanylate cyclase; cGMP; tyrosine nitration; fatty acid nitration; NO-heme; NO-metal complexes; nitrite; protein kinase C; ERK; JNK; p38MAPK; tyrosine kinase receptors; calcium OVERVIEW OF SIGNALING BY REACTIVE SPECIESUnderstanding of the roles of reactive oxygen species (ROS), reactive nitrogen species (RNS) and the lipid peroxidation product, 4-hydroxy-2-nonenal (HNE) in signaling has evolved rapidly during the last decade. This has been markedly helped by identification of the specific targets in signaling pathways. In previous reviews, we defined how ROS, H 2 O 2 in particular,

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Section: Signaling Pathways Activated By Hnementioning

confidence: 99%

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

Forman

Fukuto

Miller

et al. 2008

Archives of Biochemistry and Biophysics

Self Cite

217

165

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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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“…Synthesis of GSH can be increased by raising levels of glutamate cysteine ligase (GCL) [48][49][50], the rate-limiting enzyme in GSH synthesis. GCL activity depends on the intracellular availability of cysteine, so increasing cysteine levels can partially overcome the normally tight regulatory feedback inhibition of GSH synthesis [42,[47][48][49].…”

Section: Antioxidants In the Airway Lumen Mucinmentioning

confidence: 99%

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

Cantin

White

Cross

et al. 2007

Free Radical Biology and Medicine

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Although great strides are being made in the care of individuals with cystic fibrosis (CF), this condition remains the most common fatal hereditary disease in North America. Numerous links exist between progression of CF lung disease and oxidative stress. The defect in CF is the loss of function of the transmembrane conductance regulator (CFTR) protein; recent evidence that CFTR expression and function are modulated by oxidative stress suggests that the loss may result in a poor adaptive response to oxidants. Pancreatic insufficiency in CF also increases susceptibility to deficiencies in lipophilic antioxidants. Finally the airway infection and inflammatory processes in the CF lung are potential sources of oxidants that can affect normal airway physiology and contribute to the mechanisms causing characteristic changes associated with bronchiectasis and loss of lung function. These multiple abnormalities in the oxidant/antioxidant balance raise several possibilities for therapeutic interventions that must be carefully assessed. IntroductionCystic fibrosis (CF) is the most common fatal disease caused by a single gene defect in Europe and North America [1,2]. The defective gene was identified in 1989 [3][4][5] and shown to encode the cystic fibrosis trans-membrane conductance regulator protein (CFTR). CFTR is a cyclic AMP-regulated anion channel with greatest selectivity for chloride, and bicarbonate [6][7][8]. Furthermore, CFTR regulates sodium transport across epithelial membranes through interactions with the epithelial sodium channel ENaC [9], and facilitates the trans-membrane export of the small organic anionic peptide glutathione [10]. The expression of CFTR is located in the apical membrane of epithelial cells that line mucous membranes and submucosal glands ☆ A list of participants may be found in the Acknowledgments.

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4-hydroxynonenal induces glutamate cysteine ligase through JNK in HBE1 cells

Cited by 112 publications

References 56 publications

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

The chemistry of cell signaling by reactive oxygen and nitrogen species and 4-hydroxynonenal

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

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

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