Induction of Notch signaling by tumor necrosis factor in rheumatoid synovial fibroblasts

Ando, Kiichiro; Kanazawa, Susumu; Tetsuka, T.; Ohta, Shusuke; Jiang, Xu; Tada, Toyohiro; Kobayashi, Mariko; Matsui, Nobuo; Okamoto, Takashi

doi:10.1038/sj.onc.1206965

Cited by 114 publications

(103 citation statements)

References 31 publications

(24 reference statements)

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“…TNF-a has been reported to show an increased expression in OSCC specimens 27 and promote S2 cleavage (resulting in NICD Notch1 in oral squamous cell carcinoma R Yoshida et al production) via TACE maturation in Notch signaling. [28][29][30] As shown in Figure 5, NICD cleavages were observed in a TNF-a concentration-dependent manner. In addition, NICD cleavage was inhibited by GSI treatment.…”

Section: Tnf A-dependent Oscc Cell Invasivenessmentioning

confidence: 77%

The pathological significance of Notch1 in oral squamous cell carcinoma

Yoshida

Nagata

Nakayama

et al. 2013

Laboratory Investigation

102

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Section: Tnf A-dependent Oscc Cell Invasivenessmentioning

confidence: 77%

The pathological significance of Notch1 in oral squamous cell carcinoma

Yoshida

Nagata

Nakayama

et al. 2013

Laboratory Investigation

102

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“…Overexpression of the NF-κB members c-Rel or p65 has been shown to induce J1 expression on HELA cells, whereas a NF-κB dominant negative form suppresses it [47]. Similarly, another group reported the upregulation of N1, N4 and J2 by TNFα on rheumatoid synovial fibroblasts [48]. On the other hand, numerous in vitro and in vivo studies have demonstrated the ability of Notch to expand stem/multipotential progenitors [49].…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α and endothelial cells modulate Notch signaling in the bone marrow microenvironment during inflammation

Fernández

Rodríguez

Huang

et al. 2008

Experimental Hematology

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Objective-Homeostasis of the hematopoietic compartment is challenged and maintained during conditions of stress by mechanisms that are poorly defined. To understand how the bone marrow (BM) microenvironment influences hematopoiesis, we explored the role of Notch signaling and bone marrow endothelial cells in providing microenvironmental cues to hematopoietic cells in the presence of inflammatory stimuli.Methods-The human BM endothelial cell line BMEC and primary human BM endothelial cells were analyzed for expression of Notch ligands and the ability to expand hematopoietic progenitors in an in vitro co-culture system. In vivo experiments were carried out to identify modulation of Notch signaling in BM endothelial and hematopoietic cells in mice challenged with TNFα or LPS, or in Tie2-tmTNFα transgenic mice characterized by constitutive TNFα activation.Results-BM endothelial cells were found to express Jagged ligands and to greatly support progenitor's colony-forming ability. This effect was markedly decreased by Notch antagonists and augmented by increasing levels of Jagged2. Physiologic upregulation of Jagged2 expression on BMEC was observed upon TNFα activation. Injection of TNFα or LPS upregulated 3 to 4 fold Jagged2 expression on murine BM endothelial cells in vivo and resulted in increased Notch

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“…For immunohistochemical staining, the avidin-biotin-peroxidase complex (ABC) method was used according to protocols from the manufacturer (Vector Laboratories, Burlingame, CA) (37). Paraffin sections were rehydrated and washed with tap water for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Aberrant MHC class II expression in mouse joints leads to arthritis with extraarticular manifestations similar to rheumatoid arthritis

Kanazawa¹,

Ota²,

Sekine

et al. 2006

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

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Genetic susceptibility to rheumatoid arthritis (RA) is associated with certain MHC class II molecules. To clarify the role of these determinants in RA, we generated the D1CC transgenic mouse that expressed genes involved in antigen processing and presentation by the MHC class II pathway in joints. The class II transactivator, which was transcribed from the rat collagen type II promoter and enhancer, directed the expression of these genes. In D1CC mice congenic for the H-2 q (DBA͞1) background, small amounts of bovine collagen type II in adjuvant induced reproducibly an inflammatory arthritis resembling RA. Importantly, these stimuli had no effect in DBA͞1 mice. Eighty-nine percent of D1CC mice developed chronic disease with joint swelling, redness, and heat in association with synovial proliferation as well as pannus formation and mononuclear infiltration of synovial membranes. Granulomatous lesions resembling rheumatoid nodules and interstitial pneumonitis also were observed. As in patients with RA, anticyclic citrullinated peptide antibodies were detected during the inflammatory stage. Finally, joints in D1CC mice displayed juxtaarticular demineralization, severe joint space narrowing, and erosions, which led to ankylosis, but without the appearance of osteophytes. Thus, aberrant expression of MHC class II in joints facilitates the development of severe erosive inflammatory polyarthritis, which is very similar to RA. autoimmunity ͉ class II transactivator ͉ transgenic mouse ͉ nodules ͉ pneumonitis R heumatoid arthritis (RA) is a chronic inflammatory disease with symmetrical inflammatory and erosive polyarthritis of synovial joints and a variety of extraarticular manifestations. Particular MHC class II alleles such as DRB0401, DRB0404, and DQ8 are linked to RA in 30-50% of cases (1-3). To examine possible mechanisms of RA, many models of inflammatory arthritis have been developed in the mouse and rat (4, 5). Among these models, collagen-induced arthritis (CIA) leads to acute inflammation, osteophytosis, and destruction of bone in DBA͞1 and B10.Q (H2 q ) strains of mice (6, 7). In these mice, passively transferred autoantibodies against CII, or the injection of a combination of certain monoclonal anti-CII antibodies, also induce rapid inflammation of joints (8,9). A recently discovered model, the SKG mouse, contains mutations in the chainassociated protein of 70 kDa (ZAP-70) that is involved in the signaling from the T cell antigen receptor (10). In these mice, infection with fungi or immunization with zymosan can induce a chronic inflammatory arthritis (11). In K͞BxN mice, chronic arthritis develops spontaneously because anti-G6PI antibodies accumulate in serum and joints, leading to inflammatory arthritis and bone destruction (12,13). In all these mice and several other models, the onset and progression of inflammatory arthritis have been well characterized and analyzed. However, how faithfully these small animal models resemble RA and what roles MHC class II play in their disease have remained elusive.MHC cla...

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Induction of Notch signaling by tumor necrosis factor in rheumatoid synovial fibroblasts

Cited by 114 publications

References 31 publications

The pathological significance of Notch1 in oral squamous cell carcinoma

The pathological significance of Notch1 in oral squamous cell carcinoma

Tumor necrosis factor-α and endothelial cells modulate Notch signaling in the bone marrow microenvironment during inflammation

Aberrant MHC class II expression in mouse joints leads to arthritis with extraarticular manifestations similar to rheumatoid arthritis

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