Attenuation of interleukin-8 production by inhibiting nuclear factor-κB translocation using decoy oligonucleotides∗

Cooper, John A.; Parks, Jane M.; Carcelen, Roxanna; Kahlon, Summerpal S.; Sheffield, Michael; Culbreth, Rachel

doi:10.1016/s0006-2952(99)00375-5

Cited by 29 publications

(17 citation statements)

References 19 publications

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“…Neither z-VAD-fmk nor Boc-D-fmk (3-300 M) affected TNFRI or TNFRII expression in vehicle (3% Ϯ 1% and 0.5% Ϯ 0.5% at 300 M, respectively) or TNF␣-treated cells (98% Ϯ 2% and 92.4% Ϯ 4% at 300 M, respectively). Likewise, using interleukin-8 (IL-8) secretion as a readout of TNF␣-stimulated NF-B activation, [14][15][16] z-VAD-fmk, Boc-D-fmk, and z-IETD-fmk all failed to modify the release of IL-8 (data not shown), a finding that concurs with Liu and coworkers. 3…”

Section: Effects Of Z-vad-fmk On Tnfri/ii Expression and Tnf␣-mediatesupporting

confidence: 84%

z-VAD-fmk augmentation of TNFα-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species

Cowburn

White

Deighton

et al. 2005

Blood

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In most cell types constitutive and ligandinduced apoptosis is a caspase-dependent process. In neutrophils, however, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-␣ (TNF␣)-induced cell death, and this has been interpreted as evidence for caspase-dependent and -independent cell death pathways. Our aim was to determine the specificity of the effect of z-VADfmk in neutrophils and define the potential mechanism of action. While confirming that z-VAD-fmk (> 100 M) enhances TNF␣-induced neutrophil apoptosis, lower concentrations (1-30 M) completely blocked TNF␣-stimulated apoptosis. Boc-D-fmk, a similar broad-spectrum caspase inhibitor, and z-IETD-fmk, a selective caspase-8 inhibitor, caused a concentration-dependent inhibition of only TNF␣-stimulated apoptosis. Moreover, the caspase-9 inhibitor, Ac-LEHDcmk, had no effect on TNF␣-induced apoptosis, and z-VAD-fmk and Boc-D-fmk inhibited TNF␣-stimulated reactive oxygen species (ROS) generation. These data suggest that TNF␣-induced apoptosis in neutrophils is fully caspase dependent and uses a mitochondrial-independent pathway and that the proapoptotic effects of z-VAD-fmk are compound specific and ROS independent. (Blood. 2005;105: 2970-2972)

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Section: Effects Of Z-vad-fmk On Tnfri/ii Expression and Tnf␣-mediatesupporting

confidence: 84%

z-VAD-fmk augmentation of TNFα-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species

Cowburn

White

Deighton

et al. 2005

Blood

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“…Second, administration of NF B decoy markedly inhibits myocardial cell infiltration, which may be Gene Therapy regulated by the inflammatory network which includes cytokines and chemokines. 7 In the latest studies, NF B decoy attenuates IL-8 which is a polymorphonuclear neutrophil chemotaxin, 25 and in vivo administration of NF B decoy reduces monocyte infiltration and VCAM-1 expression in a rat renal transplant model. 26 Therefore, NF B is one of the key regulators promoting acute rejection; the decoy strategy against NF B may provide …”

Section: Discussionmentioning

confidence: 99%

Decoy against nuclear factor-kappa B attenuates myocardial cell infiltration and arterial neointimal formation in murine cardiac allografts

et al. 2000

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Acute rejection and graft arteriopathy in cardiac transplantation limit the long-term survival of recipients; these processes are enhanced by several cytokines and adhesion molecules. Nuclear factor-kappa B (NF B) is critical in the transcription of multiple genes involved in inflammation and cell proliferation. To test the hypothesis that NF B decoy can attenuate acute rejection and arteriopathy, we performed single intraluminal delivery of NF B decoy into murine cardiac allografts using a hemagglutinating virus of Japan (HVJ)-artificial viral envelope (AVE)-liposome method. No decoy or scrambled decoy transfer was performed for control. Hearts were heterotopically transplanted from BALB/c to C3H/He mice (major mismatch group) and from DBA/2 to

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“…Both double-stranded and single-stranded oligonucleotides forming either linear or hairpin selfcomplementary sequences [112] have been shown to selectively affect transcription in cells [153][154][155][156][157]. An advantage of this approach is that the construction of the binding sequences is not limited to polypurine or polypyrimidine tracts, as in the case of triple helix forming oligonucleotides [105].…”

Section: Triple Helicesmentioning

confidence: 99%

Transcription Factors As Targets for DNA-Interacting Drugs

Gniazdowski¹,

Denny²,

Nelson³

et al. 2003

CMC

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Gene expression, both tissue specific or inducible, is controlled at the level of transcription by various transcription factors interacting with specific sequences of DNA. Anticancer drugs and other potential therapeutic agents alter interactions of regulatory proteins with DNA by a variety of different mechanisms. The main ones, considered in the review, are: i) competition for the transcription factor DNA binding sequences by drugs that interact non-covalently with DNA (e.g. anthracyclines, acridines, actinomycin D, pyrrole antibiotics and their polyamide derivatives); ii) covalent modifications of DNA by alkylating agents (e.g. nitrogen mustards, cisplatin) that prevent transcription factors from recognizing their specific sequences, or that result in multiple "unnatural" binding sites in DNA which hijack the transcription factors, thus decreasing their availability in the nucleus; iii) competition with binding sites on the transcription factors by synthetic oligonucleotides or peptide nucleic acids in an antigene strategy. The latter compounds may also compete for binding sites on regulatory proteins, acting as decoys to lower their active concentration in the cell. In this review, we have summarized recent advances which have been made towards understanding the above mechanisms by which small molecules interfere with the function of transcription factors.

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Attenuation of interleukin-8 production by inhibiting nuclear factor-κB translocation using decoy oligonucleotides∗

Cited by 29 publications

References 19 publications

z-VAD-fmk augmentation of TNFα-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species

z-VAD-fmk augmentation of TNFα-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species

Decoy against nuclear factor-kappa B attenuates myocardial cell infiltration and arterial neointimal formation in murine cardiac allografts

Transcription Factors As Targets for DNA-Interacting Drugs

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