Different effects of oxidative stress on activation of transcription factors in primary cultured rat neuronal and glial cells

Iwata, Emi; Asanuma, Masato; Nishibayashi, Sakiko; Kondo, Yoichi; Ogawa, Norio

doi:10.1016/s0169-328x(97)00190-3

Cited by 44 publications

(35 citation statements)

References 40 publications

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“…Recent studies show that H 2 O 2 regulates the activity of CREB in astrocytes (25), glial cells (26), macrophages (27), and smooth muscle cells (28). The present study indicates that H 2 O 2 also serves to activate CREB in lung epithelial cells.…”

Section: Changes In Intracellular Casupporting

confidence: 67%

Oxidant-Mediated cAMP Response Element Binding Protein Activation

Barlow

Shukla²,

Mossman³

et al. 2006

Am J Respir Cell Mol Biol

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Section: Changes In Intracellular Casupporting

confidence: 67%

Oxidant-Mediated cAMP Response Element Binding Protein Activation

Barlow

Shukla²,

Mossman³

et al. 2006

Am J Respir Cell Mol Biol

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“…Several mechanisms by which oxidative stress could decrease BDNF have been suggested, including decreased CREB, increased NF-kB DNA-binding activity 8,9 or energy depletion. 7 Notably, decreased CREB levels and increased NF-kB gene expression have been found in postmortem brains of BD subjects 10,11 and an energy crisis due to mitochondrial dysfunction has been implicated in the pathophysiology of BD.…”

Section: Discussionmentioning

confidence: 99%

Increased oxidative stress as a mechanism for decreased BDNF levels in acute manic episodes

Kapczinski

Frey

Andreazza

et al. 2008

Rev. Bras. Psiquiatr.

135

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“…This transcription factor was reported to be activated by H 2 O 2 in nonphagocytic cells (14,15), and it has been shown to be important for chemokine regulation (29,32). Based on these observations, we initially tested the capacity of H 2 O 2 to activate CREB in M. As illustrated in Fig.…”

Section: Identification Of H 2 O 2 -Activated Transcription Factors Imentioning

confidence: 99%

“…In addition to its kinase-activating role, several studies show that H 2 O 2 directly regulates the activity of various transcription factors, including CREB in astrocytes (14) and glial cells (15), as well as the reduction-oxidation (redox)-sensitive transcription factors NF-B (16,17) and AP-1 (18,19) in a variety of cell types. Of interest, activation of AP-1 and NF-B transcription factors has been associated with ROS-dependent chemokine induction.…”

mentioning

confidence: 99%

Hydrogen Peroxide Induces Murine Macrophage Chemokine Gene Transcription Via Extracellular Signal-Regulated Kinase- and Cyclic Adenosine 5′-Monophosphate (cAMP)-Dependent Pathways: Involvement of NF-κB, Activator Protein 1, and cAMP Response Element Binding Protein

Jaramillo

Olivier

2002

The Journal of Immunology

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Hydrogen peroxide (H2O2) has been shown to act as a second messenger that activates chemokine expression. In the present study, we investigated the mechanisms underlying this cellular regulation in the murine macrophage cell line B10R. We report that H2O2 increases mRNA expression of various chemokines, macrophage-inflammatory protein (MIP)-1α/CC chemokine ligand (CCL)3, MIP-1β/CCL4, MIP-2/CXC chemokine ligand 2, and monocyte chemoattractant protein-1/CCL2, by activating the extracellular signal-regulated kinase (ERK) pathway and the nuclear translocation of the transcription factors NF-κB, AP-1, and CREB. Blockage of the ERK pathway with specific inhibitors against mitogen-activated protein kinase kinase 1/2 and ERK1/ERK2 completely abolished both the H2O2-mediated chemokine up-regulation and the activation of all NF studied. Similarly, selective inhibition of cAMP and NF-κB strongly down-regulated the induction of all chemokine transcripts as well as CREB and NF-κB activation, respectively. Of interest, we detected a significant decrease of NF-κB, AP-1, and CREB DNA binding activities by reciprocal competition for these binding sites when either specific cold oligonucleotides (NF-κB, AP-1, and CREB) or Abs against various transcription factor subunits (p50, p65, c-Fos, Jun B, c-Jun, and CREB-1) were added. These findings indicate that cooperation between ERK- and cAMP-dependent pathways seems to be required to achieve the formation of an essential transcriptional factor complex for maximal H2O2-dependent chemokine modulation. Finally, experiments performed with actinomycin D suggest that H2O2-mediated MIP-1β mRNA up-regulation results from transcriptional control, whereas that of MIP-1α, MIP-2, and monocyte chemoattractant protein-1 is due to both gene transcription activation and mRNA posttranscriptional stabilization.

show abstract

Different effects of oxidative stress on activation of transcription factors in primary cultured rat neuronal and glial cells

Cited by 44 publications

References 40 publications

Oxidant-Mediated cAMP Response Element Binding Protein Activation

Oxidant-Mediated cAMP Response Element Binding Protein Activation

Increased oxidative stress as a mechanism for decreased BDNF levels in acute manic episodes

Hydrogen Peroxide Induces Murine Macrophage Chemokine Gene Transcription Via Extracellular Signal-Regulated Kinase- and Cyclic Adenosine 5′-Monophosphate (cAMP)-Dependent Pathways: Involvement of NF-κB, Activator Protein 1, and cAMP Response Element Binding Protein

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