REGULATION OF IL-1-INDUCED GINGIVAL COLLAGENASE GENE EXPRESSION BY ACTIVATOR PROTEIN-1 (c-FOS/c-JUN)

Hamid, QA; Reddy, P. Jagan Mohan; Tewari, Manorama; Uematsu, Satoko; Tuncay, O.C.; Tewari, D S

doi:10.1006/cyto.2000.0676

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…In the present study, we demonstrated that IL‐1β rapidly stimulates the phosphorylation of each of these in HPL cells. Furthermore, it was previously shown that IL‐1 and TNF‐α enhance AP‐1 DNA binding activity in gingival fibroblasts and synovial fibroblasts (14–16) and, after binding to AP‐1 binding sites in promoters, AP‐1 activates the transcription of various target genes in response to cytokines (17). We also found that IL‐1β treatment of HPL cells resulted in the enhancement of AP‐1 DNA binding.…”

Section: Discussionmentioning

confidence: 99%

MAPKs, activator protein-1 and nuclear factor-κB mediate production of interleukin-1β-stimulated cytokines, prostaglandin E2 and MMP-1 in human periodontal ligament cells

Murayama

Kobayashi

Takeshita

et al. 2011

Journal of Periodontal Research

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Section: Discussionmentioning

confidence: 99%

MAPKs, activator protein-1 and nuclear factor-κB mediate production of interleukin-1β-stimulated cytokines, prostaglandin E2 and MMP-1 in human periodontal ligament cells

Murayama

Kobayashi

Takeshita

et al. 2011

Journal of Periodontal Research

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“…AP‐1 is implicated in at least two important processes that lead to periodontal disease. Besides its requirement in the expression of several cytokines (see above), it also regulates the expression of MMPs in response to IL‐1β (92). IL‐1β is a multifunctional cytokine that stimulates the production of various factors such as MMPs, NOS, or other cytokines.…”

Section: Inflammatory Bone and Joint Diseasesmentioning

confidence: 99%

Fos/AP‐1 proteins in bone and the immune system

Wagner

Eferl

2005

Immunological Reviews

473

358

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The skeleton and the immune system share a variety of different cytokines and transcription factors, thereby mutually influencing each other. These interactions are not confined to the bone marrow cavity where bone cells and hematopoietic cells exist in proximity but also occur at locations that are target sites for inflammatory bone diseases. The newly established research area termed 'osteoimmunology' attempts to unravel these skeletal/immunological relationships. Studies towards a molecular understanding of inflammatory bone diseases from an immunological as well as a bone-centered perspective have been very successful and led to the identification of several signaling pathways that are causally involved in inflammatory bone loss. Induction of receptor activator of nuclear factor (NF)-kappaB ligand (RANKL) signals by activated T cells and subsequent activation of the key transcription factors Fos/activator protein-1 (AP-1), NF-kappaB, and NF for activation of T cells c1 (NFATc1) are in the center of the signaling networks leading to osteoclast-mediated bone loss. Conversely, nature has employed the interferon system to antagonize excessive osteoclast differentiation, although this counteracting activity appears to be overruled under pathological conditions. Here, we focus on Fos/AP-1 functions in osteoimmunology, because this osteoclastogenic transcription factor plays a central role in inflammatory bone loss by regulating genes like NFATc1 as well as the interferon system. We also attempt to put potential therapeutic strategies for inflammatory bone diseases in perspective.

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“…Another transcription factor that plays a major role in periodontal diseases is the activator protein‐1 (22). Activator protein‐1 and NF‐κB both regulate the expression of matrix metalloproteinases, TGF‐β, keratinocyte growth factor and many other molecules in epithelial cells and fibroblasts (57, 62, 120, 147, 151). They also mediate lipopolysaccharide‐induced gene transcription (110, 148).…”

Section: Biochemical Signaling Events Activated In Inflammation and Fmentioning

confidence: 99%

Molecular and cell biology of healthy and diseased periodontal tissues

Bartold

Narayanan²

2006

Periodontology 2000

146

142

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REGULATION OF IL-1-INDUCED GINGIVAL COLLAGENASE GENE EXPRESSION BY ACTIVATOR PROTEIN-1 (c-FOS/c-JUN)

Cited by 14 publications

References 34 publications

MAPKs, activator protein-1 and nuclear factor-κB mediate production of interleukin-1β-stimulated cytokines, prostaglandin E2 and MMP-1 in human periodontal ligament cells

MAPKs, activator protein-1 and nuclear factor-κB mediate production of interleukin-1β-stimulated cytokines, prostaglandin E2 and MMP-1 in human periodontal ligament cells

Fos/AP‐1 proteins in bone and the immune system

Molecular and cell biology of healthy and diseased periodontal tissues

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