Inhibition of intimal hyperplasia after balloon injury in rat carotid artery model using cis-element ‘decoy’ of nuclear factor-kB binding site as a novel molecular strategy

Yoshimura, Shin; Morishita, Ryuichi; Hayashi, Kozaburo; Yamamoto, Kei; Nakagami, Hironori; Kaneda, Yasufumi; Sakai, Noboru; Ogihara, Toshio

doi:10.1038/sj.gt.3301566

Cited by 123 publications

(100 citation statements)

References 37 publications

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“…The relation of NF-B activation to cellular dysfunction and vascular disease has been directly established by using genetic approaches to overexpress the NF-Bspecific inhibitor I B␣ (28) and by indirect studies looking at the presence of cells with nuclear located NF-B in vascular disease (24)(25)(26)(27)29). A cooperative action of catecholamines regulating receptor expression and other stress response modifiers might act in concert in controlling cell activation.…”

Section: Discussionmentioning

confidence: 99%

“…One observation pointing to a potential mechanism is the induction of inflammatory reactions and the simultaneous decrease of antiinflammatory reactions leading to enhanced cytokine release and monocytic cell activation (19)(20)(21)(22)(23). These changes in mononuclear properties are consistent with the activation of the redox-sensitive transcription factor nuclear factor B (NF-B) (24)(25)(26)(27)(28)(29).…”

mentioning

confidence: 97%

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A mechanism converting psychosocial stress into mononuclear cell activation

Bierhaus

Wolf

Andrassy

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

819

542

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Little is known about the mechanisms converting psychosocial stress into cellular dysfunction. Various genes, up-regulated in atherosclerosis but also by psychosocial stress, are controlled by the transcription factor nuclear factor B (NF-B). Therefore, NF-B is a good candidate to convert psychosocial stress into cellular activation. Volunteers were subjected to a brief laboratory stress test and NF-B activity was determined in peripheral blood mononuclear cells (PBMC), as a window into the body and because PBMC play a role in diseases such as atherosclerosis. In 17 of 19 volunteers, NF-B was rapidly induced during stress exposure, in parallel with elevated levels of catecholamines and cortisol, and returned to basal levels within 60 min. To model this response, mice transgenic for a strictly NF-B-controlled ␤-globin transgene were stressed by immobilization. Immobilization resulted in increased ␤-globin expression, which could be reduced in the presence of the ␣1-adrenergic inhibitor prazosin.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

A mechanism converting psychosocial stress into mononuclear cell activation

Bierhaus

Wolf

Andrassy

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

819

542

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show abstract

“…To resolve this issue, researchers have used end-modifications or conjugation of ODNs to increase their biological half life. [61][62][63][64] Further, viral envelopes including HVJ have been used to deliver ODNs in vivo, however, their safety remains unknown. 33,34,38 In the present study, injection of scrambled or decoy ODNs at 5, 20, or 40 mg per mouse did not show any influence on BW changes in mice without DSS treatment, thus those doses were considered to be safe for use in treatment of experimental colitis.…”

Section: Effects Of Decoy Odns On Expression Of Proinflammatory Cytokmentioning

confidence: 99%

Decoy oligodeoxynucleotide targeting activator protein-1 (AP-1) attenuates intestinal inflammation in murine experimental colitis

Moriyama

Ishihara

Rumi

et al. 2008

Laboratory Investigation

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Various therapies are used for inflammatory bowel diseases (IBD), though none seem to be extremely effective. AP-1 is a major transcription factor that upregulates genes involved in immune and proinflammatory responses. We investigated decoy oligodeoxynucleotide (ODN) targeting AP-1 to prevent dextran sulfate sodium (DSS)-induced colitis in mice. Functional efficacies of synthetic decoy and scrambled ODNs were evaluated in vitro by a reporter gene luciferase assay and measuring flagellin-induced IL-8 expression by HCT-15 cells transfected with ODNs. Experimental colitis was induced in mice with a 2.5% DSS solution in drinking water for 7 days, and decoy or scrambled ODNs were intraperitoneally injected from days 2 to 5. Colitis was assessed by weight loss, colon length, histopathology, and detection of myeloperoxidase (MPO), IL-1b, and TNF-a in colon tissue. Therapeutic effects of AP-1 and NF-kB decoy ODNs were compared. Transfection of AP-1 decoy ODN inhibited AP-1 transcriptional activity in reporter assays and flagellin-induced IL-8 production in vitro. In mice, AP-1 decoy ODN, but not scrambled ODN, significantly inhibited weight loss, colon shortening, and histological inflammation induced by DSS. Further, AP-1 decoy ODN decreased MPO, IL-1b, and TNF-a in colonic tissue of mice with DSS-induced colitis. The AP-1 decoy therapeutic effect was comparable to that of NF-kB decoy ODN, which also significantly decreased intestinal inflammation. Double-strand decoy ODN targeting AP-1 effectively attenuated intestinal inflammation associated with experimental colitis in mice, indicating the potential of targeting proinflammatory transcription factors in new therapies for IBD.

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“…Oxidative stress induces various cytokines, including tumor necrosis factor-(TNF-) (Guha et al, 2000). The stimulation of vascular cells by TNF-initiates a signaling cascade leading to increases in nuclear factor-B (NF-B)-dependent expression of various genes (Bourcier et al, 1997;Dhawan et al, 1997), which play pivotal roles in the formation of neointimal hyperplasia leading to restenosis following angioplasty (Yoshimura et al, 2001). α-Lipoic acid (ALA, 1,2-dithiolane-3-pentanoic acid) is a naturally occurring antioxidant which inhibits TNF--induced NF-B activation and acts as a direct free-radical scavenger (Packer et al, 1995;Zhang and Frei, 2001).…”

Section: Introductionmentioning

confidence: 99%

α-Lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-κB transcriptional activity

Kim

Kim²,

Park³

et al. 2007

Exp Mol Med

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Abbreviations: ALA, α-lipoic acid; AP-1, activator protein-1; MMP-9, matrix metalloproteinase-9; VSMC, vascular smooth muscle cell AbstractThe migration of vascular smooth muscle cells (VSMCs) into the intima, an important step in injury-induced neointimal hyperplasia, requires the activation of nuclear factor-κB (NF-κB) and the consequent up-regulation of matrix metalloproteinase-9 (MMP-9). This study was undertaken to test for a possible effect of α-lipoic acid (ALA), a potent inhibitor of NF-κB, on MMP-9 expression. ALA inhibited high-glucose-and TNF-α-stimulated VSMC migrations in vitro. It also inhibited high-glucoseand TNF-α-induced increases in MMP-9 expression. The activity of MMP-9-promoter constructs with mutations in the NF-κB binding site was not inhibited by ALA, indicating an involvement of the NF-κB signaling pathway in the ALA-specific inhibition of MMP-9. These data suggest the possibility that ALA may be useful for the prevention of neointimal hyperplasia after angioplasty, by inhibiting the NF-κB/ MMP-9 pathway, especially with hyperglycemia.

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Inhibition of intimal hyperplasia after balloon injury in rat carotid artery model using cis-element ‘decoy’ of nuclear factor-kB binding site as a novel molecular strategy

Cited by 123 publications

References 37 publications

A mechanism converting psychosocial stress into mononuclear cell activation

A mechanism converting psychosocial stress into mononuclear cell activation

Decoy oligodeoxynucleotide targeting activator protein-1 (AP-1) attenuates intestinal inflammation in murine experimental colitis

α-Lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-κB transcriptional activity

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