Mitogen-activated Protein Kinases Mediate Activator Protein-1-dependent Human Inducible Nitric-oxide Synthase Promoter Activation

Kristof, Arnold S.; Marks-Kończalik, Joanna; Moss, Joel

doi:10.1074/jbc.m009563200

Cited by 156 publications

(124 citation statements)

References 60 publications

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“…In human, a 7.2-kb segment confers partial inducibility of iNOS in response to cytokines (Taylor et al, 1998). For higher level of activation of iNOS in human, a promoter segment of 8.3 or 16 kb is required (Kristof et al, 2001;Taylor and Geller, 2000). We, in our laboratory, have observed differential activation of a 7.2 and 8.8-kb human iNOS promoter in astrocytes.…”

Section: In the Nux: Nuclear Eventsmentioning

confidence: 75%

Signals for the induction of nitric oxide synthase in astrocytes

Saha

Pahan

2006

Neurochemistry International

100

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Nitric oxide (NO), being a double-edged sword depending on its concentration in the microenvironment, is involved in both physiological and pathological processes of many organ systems including brain and spinal cord. It is now well-documented that once inducible nitric oxide synthase (iNOS) is expressed in CNS in a signal-dependent fashion, NO in excess of physiological thresholds is produced and this excess NO then plays a role in the pathogenesis of stroke, demyelination and other neurodegenerative diseases. Therefore, a keen interest has been generated in recent years in comprehending the regulation of this enzyme in brain cells. The present review summarizes our current understanding of signaling mechanisms leading to transcription of the iNOS gene in activated astrocytes. We attempt this comprehension with a hope to identify potential targets to intervene NO-mediated CNS disorders.

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Section: In the Nux: Nuclear Eventsmentioning

confidence: 75%

Signals for the induction of nitric oxide synthase in astrocytes

Saha

Pahan

2006

Neurochemistry International

100

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“…Activation of ERK has been linked to activation of the transcription factor AP-1 (27,35), and previous studies have suggested that signaling through the B1 receptor may contribute to the regulation of gene expression (36 -38). We demonstrated that Lysdes-Arg-BK could activate AP-1 in transformed human respiratory epithelial cells (A549 and BEAS-2B).…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Functional Kinin B1 Receptors in Allergic Airway Inflammation

Christiansen

Eddleston

Woessner

et al. 2002

The Journal of Immunology

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B1 receptors are known to be induced during allergic airway inflammation in animal models. However, little is known regarding in vivo B1 receptor expression in humans. We examined B1 receptor mRNA expression in nasal tissue samples from allergic rhinitis and normal subjects. Allergic rhinitis subjects displayed significantly higher expression of B1 receptor mRNA than did the normal subjects, and nasal allergen challenge increased B1 receptor mRNA expression at 8 to 24 h time points in allergic rhinitis subjects. No significant difference was found in B2 receptor expression. To confirm B2 and B1 receptor functional activity, subjects were challenged with kinin agonists. Nasal challenge with the B1 receptor ligand, Lys-des-Arg-bradykinin (BK), activated extracellular signal-regulated kinase in allergic rhinitis, but not normal, subjects. Nasal challenge with the B2 receptor ligand, BK, activated extracellular signal-regulated kinase in both allergic rhinitis and normal subjects. The consequences of B1 receptor activation were investigated using the human airway epithelial cell lines A549 and BEAS-2B. We demonstrated that Lys-des-Arg-BK activates the transcription factor AP-1. Taken together, these results show that functional B1 receptors are induced in the airway during allergic inflammation and suggest that they participate in the regulation of gene expression.

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“…The expression of iNOS (NOS-2) is regulated by all three MAP kinase pathways in a variety of cell types [16,32,46,93,108,189]. For example, JNK and ERK1/2 pathways are necessary for lipopolysaccharide (LPS)-and interferon-␥-stimulated iNOS expression in mouse macrophage cells, possibly via ␣-tumor necrosis factor secretion, whereas p38 inhibited induction [31].…”

Section: Nitric Oxide and Mapk Signalingmentioning

confidence: 99%

“…Recent reports demonstrated that the induction of iNOS expression following treatment with LPS or interferon-␥ [108], as well as the expression of nNOS requires the ERK1/2 signaling pathway, providing a potentially interesting link between MAPK signaling, nitric oxide production, and mitochondrial function. Since epicatechin and kaempferol have been shown to attenuate the oxidative stress-mediated activation of ERK1/2 [178] it remains to be established whether or not these flavonoids are capable of suppressing the production of NO • in neurons and glial cells in vivo as reported for iNOS in cultured macrophages [99,109,154], and what influences this may have on cellular outcomes of oxidative insults.…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

302

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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Mitogen-activated Protein Kinases Mediate Activator Protein-1-dependent Human Inducible Nitric-oxide Synthase Promoter Activation

Cited by 156 publications

References 60 publications

Signals for the induction of nitric oxide synthase in astrocytes

Signals for the induction of nitric oxide synthase in astrocytes

Up-Regulation of Functional Kinin B1 Receptors in Allergic Airway Inflammation

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

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