Nucleosomes activate NF‐κB in endothelial cells for induction of the proangiogenic cytokine IL‐8

Tanner, Jerome E.

doi:10.1002/ijc.20390

Cited by 20 publications

(14 citation statements)

References 60 publications

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“…These findings may explain why hypoxic and hypervascularized areas are often found in close proximity within tumor tissues and suggest a potential role for nucleosomes in supporting progression of disease. 38 Moreover, nucleosomes are thought to be important for evasion of tumor cells from immunosurveillance. They are incorporated by tumor cells, lymphocytes, and natural killer cells in a receptor-mediated way, are subsequently processed intracellularly, and inhibit natural killer cell-mediated lysis of tumor cells.…”

Section: Pathophysiological Relevance Of Circulating Nucleosomesmentioning

confidence: 99%

“…,38 2. Pathways of apoptotic cell deathAlthough apoptosis is regulated differently in different cell types, several components of the signaling pathways seem to be characteristic: extrinsically, apoptosis is induced by stimulation of receptors on the cellular surface; receptors such as CD95/Fas/APO-1 are activated after trimerization and transmit the apoptotic signal across the plasma membrane.…”

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confidence: 99%

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Clinical use of circulating nucleosomes

Holdenrieder¹,

Stieber²

2009

Critical Reviews in Clinical Laboratory Sciences

175

133

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Nucleosomes, complexes of DNA and histone proteins, are released from dying and stressed cells into the blood circulation. Concentrations of circulating nucleosomes in plasma and serum are frequently found to be elevated in various cancers, and also in such acute conditions as stroke, trauma, and sepsis as well as in autoimmune diseases. The first part of this review focuses on the structural and functional properties of nucleosomes, the potential sources of nucleosome release into the circulation, the metabolism of circulating nucleosomes, and their pathophysiological role in disease. It goes on to describe the relevance of circulating nucleosomes in the diagnosis and prognosis of non-malignant conditions such as sepsis, stroke, and autoimmune disease. Finally, it describes the clinical value of nucleosomes in the diagnosis, staging, prognosis, and monitoring of therapy in cancer; in particular, their potential as a new diagnostic tool for the early estimation of response to cytotoxic cancer therapy is emphasized.

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Section: Pathophysiological Relevance Of Circulating Nucleosomesmentioning

confidence: 99%

mentioning

confidence: 99%

Clinical use of circulating nucleosomes

Holdenrieder¹,

Stieber²

2009

Critical Reviews in Clinical Laboratory Sciences

175

133

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“…However, other investigators have reported that TRAIL may be involved in the control of endothelial biology without the ability to activate NF-jB and induce inflammatory markers [28][29][30]. TRAIL has been proven to induce apoptosis of tumour cells in different mouse models; however, apoptosis and necrosis of solid tumours may play an important role in the promotion of tumour angiogenesis through increased expression of CXCL8 in vascular endothelial cells following nucleosome stimulation [33]. In addition, TRAIL has been shown to up-regulate CXCL8 expression in human astroglioma cells, and Choi et al [34] and Varfolomeev et al [35] have also reported that TRAIL is able to induce CXCL8 and CCL2 secretion in both HT1080 and HT29 cells.…”

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confidence: 99%

Tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL)‐induced chemokine release in both TRAIL‐resistant and TRAIL‐sensitive cells via nuclear factor kappa B

et al. 2008

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Tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL) induces apoptosis in a variety of tumour cells, but not in most normal cells, and has attracted considerable attention for its potential use in cancer therapy. Recently, increasing evidence has shown that TRAIL is involved in inflammation, although much of this evidence is controversial. In this article, it is shown that TRAIL induces CXCL2, CCL4 and CCL20 secretion in a nuclear factor kappa B‐dependent manner. The dominant negative constructs of tumour necrosis factor receptor‐associated death domain protein (TRADD) and tumour necrosis factor receptor‐associated factor 2 are unable to block TRAIL‐induced chemokine up‐regulation, and the dominant negative construct of TRADD may even enhance TRAIL‐triggered signals. Using small interfering RNA, receptor interacting protein has been demonstrated to be essential for TRAIL‐induced chemokine release. Furthermore, it has been demonstrated that p38 mitogen‐activated protein kinase is involved in TRAIL‐induced chemokine release without any effects on nuclear factor kappa B activation, suggesting that some unknown transcription factors may be activated by TRAIL. Using a xenograft tumour model, it has been illustrated that TRAIL can also induce chemokine release in vivo. Although these chemokines induced by TRAIL are inflammatory chemokines, their functions are not restricted to inflammation and require further examination. Our results indicate that attention should be paid to the side‐effects of TRAIL treatment, not only in TRAIL‐resistant but also in TRAIL‐sensitive tumour cells.

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“…They are in direct contact with the circulating anti-dsDNA antibodies/nucleosomes and the activated effector cells. Nucleosomes have been shown to activate endothelial cells to produce proinflammatory cytokines such as IL-6 and IL-8 [51]. In addition, endothelial bound nucleosomes and C1q are targets for autoantibodies and lead to activation of complement [52].…”

Section: Tubular Cells and Microcapillary Endothelial Cellsmentioning

confidence: 99%

The effect of cell death in the initiation of lupus nephritis

Fenton

2014

Clinical and Experimental Immunology

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The effect of cell death in the initiation of lupus nephritis OTHER ARTICLES PUBLISHED IN THIS SERIESDying autologous cells as instructors of the immune system. Clinical and Experimental Immunology 2015, 179: 1-4. Anti-dsDNA antibodies as a classification criterion and a diagnostic marker for systemic lupus erythematosus: critical remarks. Clinical and Experimental Immunology 2015, 179: 5-10 SummaryCell death and the release of chromatin have been demonstrated to activate the immune system producing autoantibodies against nuclear antigens in patients with systemic lupus erythematosus (SLE). Apoptosis, necrosis, necroptosis, secondary necrosis, autophagy and the clearance of dying cells by phagocytosis are processes believed to have a role in tolerance avoidance, activation of autoimmune lymphocytes and tissue damage by effector cells. The released chromatin not only activates the immune system; it also acts as antigen for the autoantibodies produced, including anti-dsDNA antibodies. The subsequent immune complex formed is deposited within the basement membranes and the mesangial matrix of glomeruli. This may be considered as an initiating event in lupus nephritis. The origin of the released chromatin is still debated, and the possible mechanisms and cell sources are discussed in this study.

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Nucleosomes activate NF‐κB in endothelial cells for induction of the proangiogenic cytokine IL‐8

Cited by 20 publications

References 60 publications

Clinical use of circulating nucleosomes

Clinical use of circulating nucleosomes

Tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL)‐induced chemokine release in both TRAIL‐resistant and TRAIL‐sensitive cells via nuclear factor kappa B

The effect of cell death in the initiation of lupus nephritis

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