Effects of IL-1β on gene expression in human rheumatoid synovial fibroblasts

Jeong, Jae-Gyun; Kim, Jong-Mook; Cho, Hongchan; Hahn, Woong; Yu, Seung Shin; Kim, Sun‐Young

doi:10.1016/j.bbrc.2004.09.011

Cited by 58 publications

(41 citation statements)

References 17 publications

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“…Reduced expression of IL-1b in response to IL-1Ra presumably reflects the interruption of an autocrine induction loop (Abe et al, 1997). The reduced expression of MMP-3 confirms the importance of IL-1 as an inducer of this enzyme in rheumatoid joints ( Jeong et al, 2004). Additional studies, using more precise outcome measures and larger numbers of subjects who do not undergo early synovectomy, are needed to evaluate these matters further.…”

Section: Discussionmentioning

confidence: 78%

Clinical responses to gene therapy in joints of two subjects with rheumatoid arthritis

Wehling¹,

Reinecke²,

Baltzer³

et al. 2008

Human Gene Therapy

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This paper provides the first evidence of a clinical response to gene therapy in human arthritis. Two subjects with rheumatoid arthritis received ex vivo, intraarticular delivery of human interleukin-1 receptor antagonist (IL1Ra) cDNA. To achieve this, autologous synovial fibroblasts were transduced with a retrovirus, MFG-IRAP, carrying IL-1Ra as the transgene, or remained as untransduced controls. Symptomatic metacarpophalangeal (MCP) joints were injected with control or transduced cells. Joints were clinically evaluated on the basis of pain; the circumference of MCP joint 1 was also measured. After 4 weeks, joints underwent surgical synovectomy. There were no adverse events in either subject. The first subject responded dramatically to gene transfer, with a marked and rapid reduction in pain and swelling that lasted for the entire 4 weeks of the study. Remarkably, joints receiving IL-1Ra cDNA were protected from flares that occurred during the study period. Analysis of RNA recovered after synovectomy revealed enhanced expression of IL-1Ra and reduced expression of matrix metalloproteinase-3 and IL-1b. The second subject also responded with reduced pain and swelling. Thus, gene transfer to human, rheumatoid joints can be accomplished safely to produce clinical benefit, at least in the short term. Using this ex vivo procedure, the transgene persisted within the joint for at least 1 month. Further clinical studies are warranted.

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Section: Discussionmentioning

confidence: 78%

Clinical responses to gene therapy in joints of two subjects with rheumatoid arthritis

Wehling¹,

Reinecke²,

Baltzer³

et al. 2008

Human Gene Therapy

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“…MCF-7 cells (2x10 6 ) were treated with cordycepin in the presence or absence of TPA for 4 h. Cells were immediately washed twice, scraped into 1.5 ml of ice-cold PBS (pH 7.5), and pelleted at 1,500 x g for 3 min. Cytoplasmic and nuclear extracts were prepared from cells using the NE-PER ® Nuclear and Cytoplasmic Extraction Reagents (Pierce Biotechnology, Rockford, IL).…”

Section: Western Blot Analysis Mcf-7 Cells (5x10mentioning

confidence: 99%

“…Cordyceps and products are available in Western countries as over-the-counter medicine/ tonics that advertise them as Chinese herbs with anti-aging, 'pro-sexual', anti-cancer and immune-boosting effects (3). Cordycepin, which is a 3-deoxyadenosin isolated from Cordyceps, has been reported to exert inhibitory effects on macrophages based on anti-inflammatory properties (6). However, the anti-metastatic effects of cordycepin have not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

Cordycepin inhibits TPA-induced matrix metalloproteinase-9 expression by suppressing the MAPK/AP-1 pathway in MCF-7 human breast cancer cells

Noh

Youn²,

Jung³

et al. 2009

Int J Mol Med

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Abstract. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in breast cancer cell invasion. NF-κB and AP-1 are known to induce MMP-9 expression. We investigated whether cordycepin, an NF-κB or AP-1 inhibitor, can modulate MMP-9 expression and cell invasion in MCF-7 cells. Toxicity of cordycepin was determined by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. MMP-9 expression was determined by real-time PCR, Zymography, and Western blot analysis. AP-1 activation was assayed by electrophoretic mobility shift assay (EMSA). MAPK signaling was evaluated by Western blotting with specific p-ERK, and ERK, p-p38, p38, p-JNK, JNK antibodies. Cordycepin suppressed AP-1 activation, but not NF-κB activation in 12-O-tetradecanoylpho-bol-13-acetate (TPA)-treated MCF-7 cells. Cordycepin inhibits TPA-induced MMP-9 expression and cell invasion by suppressing AP-1 activation. Also, cordycepin suppressed the MAPK signaling pathway. Cordycepin is a potent inhibitor of TPA-induced MMP-9 expression and blocks strongly the ability of AP-1 activation via MAPK signaling pathway in MCF-7 cells.

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“…103 IL-1␤ decreases tissue inhibitor of metalloproteinase expression. 104 Reactive oxygen species induce tissue inhibitor of metalloproteinase activity. 105 Smoking is associated with increased TGF-␤ levels, 106 by which smoking may inhibit metalloproteinase gene expression 3 and induce tissue inhibitor of metalloproteinase expression.…”

Section: Smoking and Regulation Of Matrix Metalloproteinase Activitymentioning

confidence: 99%

Smoking, Metalloproteinases, and Vascular Disease

Perlstein

Lee

2006

ATVB

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Abstract-Smoking causes up to 11% of total global cardiovascular deaths. Smoking has numerous effects that may promote atherosclerosis through vascular inflammation and oxidative stress, but the pathogenesis of smoking-related cardiovascular disease remains incompletely understood. The matrix metalloproteinases, a family of endopeptidases that can degrade extracellular matrix components in both physiological and pathophysiological states, play an important role in smoking-associated chronic obstructive pulmonary disease, the second leading cause of smoking attributable mortality. Emerging evidence indicates that the matrix metalloproteinases may also contribute to smoking-related vascular disease. Here we discuss the potential relationship between smoking, matrix metalloproteinases, and acceleration of vascular disease.

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Effects of IL-1β on gene expression in human rheumatoid synovial fibroblasts

Cited by 58 publications

References 17 publications

Clinical responses to gene therapy in joints of two subjects with rheumatoid arthritis

Clinical responses to gene therapy in joints of two subjects with rheumatoid arthritis

Cordycepin inhibits TPA-induced matrix metalloproteinase-9 expression by suppressing the MAPK/AP-1 pathway in MCF-7 human breast cancer cells

Smoking, Metalloproteinases, and Vascular Disease

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