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RAGE signaling sustains inflammation and promotes tumor development

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RAGE signaling sustains inflammation and promotes tumor development. / Gebhardt, Christoffer; Riehl, Astrid; Durchdewald, Moritz; Németh, Julia; Fürstenberger, Gerhard; Müller-Decker, Karin; Enk, Alexander; Arnold, Bernd; Bierhaus, Angelika; Nawroth, Peter P; Hess, Jochen; Angel, Peter.

in: J EXP MED, Jahrgang 205, Nr. 2, 18.02.2008, S. 275-85.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Gebhardt, C, Riehl, A, Durchdewald, M, Németh, J, Fürstenberger, G, Müller-Decker, K, Enk, A, Arnold, B, Bierhaus, A, Nawroth, PP, Hess, J & Angel, P 2008, 'RAGE signaling sustains inflammation and promotes tumor development', J EXP MED, Jg. 205, Nr. 2, S. 275-85. https://doi.org/10.1084/jem.20070679

APA

Gebhardt, C., Riehl, A., Durchdewald, M., Németh, J., Fürstenberger, G., Müller-Decker, K., Enk, A., Arnold, B., Bierhaus, A., Nawroth, P. P., Hess, J., & Angel, P. (2008). RAGE signaling sustains inflammation and promotes tumor development. J EXP MED, 205(2), 275-85. https://doi.org/10.1084/jem.20070679

Vancouver

Gebhardt C, Riehl A, Durchdewald M, Németh J, Fürstenberger G, Müller-Decker K et al. RAGE signaling sustains inflammation and promotes tumor development. J EXP MED. 2008 Feb 18;205(2):275-85. https://doi.org/10.1084/jem.20070679

Bibtex

@article{e1aeee1ea6a841cd947684afdeb0bc9b,
title = "RAGE signaling sustains inflammation and promotes tumor development",
abstract = "A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.",
keywords = "9,10-Dimethyl-1,2-benzanthracene, Animals, Female, Gene Expression Regulation, Neoplastic, Inflammation, Macrophage Inflammatory Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptor for Advanced Glycation End Products, Receptors, Immunologic, S100 Proteins, Skin Neoplasms, Tetradecanoylphorbol Acetate, Journal Article, Research Support, Non-U.S. Gov't",
author = "Christoffer Gebhardt and Astrid Riehl and Moritz Durchdewald and Julia N{\'e}meth and Gerhard F{\"u}rstenberger and Karin M{\"u}ller-Decker and Alexander Enk and Bernd Arnold and Angelika Bierhaus and Nawroth, {Peter P} and Jochen Hess and Peter Angel",
year = "2008",
month = feb,
day = "18",
doi = "10.1084/jem.20070679",
language = "English",
volume = "205",
pages = "275--85",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - RAGE signaling sustains inflammation and promotes tumor development

AU - Gebhardt, Christoffer

AU - Riehl, Astrid

AU - Durchdewald, Moritz

AU - Németh, Julia

AU - Fürstenberger, Gerhard

AU - Müller-Decker, Karin

AU - Enk, Alexander

AU - Arnold, Bernd

AU - Bierhaus, Angelika

AU - Nawroth, Peter P

AU - Hess, Jochen

AU - Angel, Peter

PY - 2008/2/18

Y1 - 2008/2/18

N2 - A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.

AB - A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.

KW - 9,10-Dimethyl-1,2-benzanthracene

KW - Animals

KW - Female

KW - Gene Expression Regulation, Neoplastic

KW - Inflammation

KW - Macrophage Inflammatory Proteins

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Receptor for Advanced Glycation End Products

KW - Receptors, Immunologic

KW - S100 Proteins

KW - Skin Neoplasms

KW - Tetradecanoylphorbol Acetate

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1084/jem.20070679

DO - 10.1084/jem.20070679

M3 - SCORING: Journal article

C2 - 18208974

VL - 205

SP - 275

EP - 285

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 2

ER -