AP-1 and NF-kB Regulation in Rheumatoid Arthritis and Murine Collagen-Induced Arthritis

Han, Zhen; Boyle, D. L.; Manning, Anthony M.; Firestein, Gary S.

doi:10.3109/08916939808995367

Cited by 352 publications

(246 citation statements)

References 44 publications

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“…Studies on several animal models of inflammation support the notion that NF-B plays a physiologic role in inflammatory responses in vivo. For example, NF-B has been shown to be involved in carrageenan-induced pleurisy in rats (16), while synovial NF-B activation occurs within a few days after immunization in a rat adjuvant arthritis model (17) and precedes the development of clinical joint involvement in a murine collagen-induced arthritis model (18). NF-B is also highly activated at sites of inflammation in several diseases and contributes to the duration of chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…The housekeeping gene ␤-actin was used as an internal control. Total RNA (7 g) was reverse-transcribed into complementary DNA by using oligo(dT) [12][13][14][15][16][17][18] primer (Invitrogen) and Superscript II reverse transcriptase (Invitrogen). Complementary DNA (1 l) was amplified by PCR using Taq polymerase (Promega, Madison, WI) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

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Amelioration of acute inflammation by systemic administration of a cell‐permeable peptide inhibitor of NF‐κB activation

Meglio

Ianaro

Ghosh

2005

Arthritis & Rheumatism

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Objective. We used an experimental model of inflammation in mice, carrageenan-induced paw edema, to study the antiinflammatory effects of the NEMObinding domain (NBD) peptide, which blocks activation of the inducible transcription factor NF-B.Methods. Paw edema was induced by subplantar injection of 1% -carrageenan into the mouse left hind paw. Test agents were given intraperitoneally immediately after carrageenan injection. The increase in footpad thickness was considered to be edema. In some experiments, the mice were killed and the paws were removed for histologic and molecular biology analysis. NF-B DNA binding activity was evaluated in nuclear extracts by electrophoretic mobility shift assays. The expression levels of NF-B-regulated cyclooxygenase 2 (COX-2) protein and tumor necrosis factor ␣ (TNF␣) messenger RNA (mRNA) were evaluated by immunoblot analysis and polymerase chain reaction amplification of reverse-transcribed mRNA, respectively.Results. We found that systemically administered NBD peptide significantly inhibited edema formation and cellular infiltration in inflamed mouse paws. This antiinflammatory activity was most likely due to inhibition of expression of proinflammatory mediators, such as TNF␣ and COX-2, in inflamed tissues. Conclusion.These studies further establish NF-B as a target for antiinflammatory therapy and provide support for the use of the NBD peptide as a possible therapeutic agent for inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Amelioration of acute inflammation by systemic administration of a cell‐permeable peptide inhibitor of NF‐κB activation

Meglio

Ianaro

Ghosh

2005

Arthritis & Rheumatism

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“…In a murine collagen-induced arthritis and in a rat adjuvant-induced arthritis model, it has been shown that the clinical manifestation of the disease is preceded by NF-kB activation. 61 A lot of effort has been invested to understand the upstream component responsible for NF-kB activation in the synovial tissue. IKK2 is the main kinase involved in cytokine-induced NF-kB activation in fibroblast-like synoviocytes.…”

Section: Nf-jb In Arthritismentioning

confidence: 99%

NF-κB and the regulation of hematopoiesis

2006

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“…NF-jB is activated in dorsal root ganglia (DRG) after partial sciatic nerve injury and is crucial for hyperalgesia [4,20]. Thus, NF-jB is regarded as one of the most important targets for therapeutic intervention against inflammatory diseases such as rheumatoid arthritis, asthma, or inflammatory bowel disease [1,8,33,35,40].…”

Section: Introductionmentioning

confidence: 99%

Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

et al. 2009

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Nuclear factor-kappa B (NF-jB) is a gene transcriptional regulator of inflammatory cytokines. We investigated the transduction efficiency of NF-jB decoy to dorsal root ganglion (DRG), as well as the decrease in nerve injury, mechanical allodynia, and thermal hyperalgesia in a rat lumbar disc herniation model. Forty rats were used in this study. NF-jB decoy-fluorescein isothiocyanate (FITC) was injected intrathecally at the L5 level in five rats, and its transduction efficiency into DRG measured. In another 30 rats, mechanical pressure was placed on the DRG at the L5 level and nucleus pulposus harvested from the rat coccygeal disc was transplanted on the DRG. Rats were classified into three groups of ten animals each: a herniation ? decoy group, a herniation ? oligo group, and a herniation only group. For behavioral testing, mechanical allodynia and thermal hyperalgesia were evaluated. In 15 of the herniation rats, their left L5 DRGs were resected, and the expression of activating transcription factor 3 (ATF-3) and calcitonin gene-related peptide (CGRP) was evaluated immunohistochemically compared to five controls. The total transduction efficiency of NF-jB decoy-FITC in DRG neurons was 10.8% in vivo. The expression of CGRP and ATF-3 was significantly lower in the herniation ? decoy group than in the other herniation groups.Mechanical allodynia and thermal hyperalgesia were significantly suppressed in the herniation ? decoy group. NFjB decoy was transduced into DRGs in vivo. NF-jB decoy may be useful as a target for clarifying the mechanism of sciatica caused by lumbar disc herniation.

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AP-1 and NF-kB Regulation in Rheumatoid Arthritis and Murine Collagen-Induced Arthritis

Abstract: The DNA binding activity of AP-1 and NF-kappaB are markedly increased in both CIA and RA. In CIA, activation of AP-1 and NF-kappaB precede both clinical arthritis and metalloproteinase gene expression. NF-kappaB expression correlated better than AP-1 with metalloproteinase expression.

Cited by 352 publications

References 44 publications

Amelioration of acute inflammation by systemic administration of a cell‐permeable peptide inhibitor of NF‐κB activation

Amelioration of acute inflammation by systemic administration of a cell‐permeable peptide inhibitor of NF‐κB activation

NF-κB and the regulation of hematopoiesis

Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

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