Receptor of advanced glycation end product (RAGE) expression in the minor salivary glands of patients with Sjo˝gren's syndrome: a preliminary study

Katz, Joseph; Stavropoulos, Franci; Bhattacharyya, Indraneel; Stewart, Carol M.; Perez, Federico M.; Caudle, Robert M.

doi:10.1080/03009740310004775

Cited by 24 publications

(25 citation statements)

References 16 publications

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“…Egr-1 is developmentally regulated and binds the GC-rich sequence GCG(G/T)GGGCG, which often overlaps the DNA-binding sequence of stimulating protein 1. Competition between stimulating protein 1 and Egr-1 leads to either activation or suppression of common target genes (15,21). Egr-1 is a crucial regulator of cell proliferation, differentiation, and survival after induction by several stimuli such as growth factors, cytokines, radiation, apoptosis-promoting factors, injury, and stretch (4,15,27).…”

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confidence: 99%

“…Competition between stimulating protein 1 and Egr-1 leads to either activation or suppression of common target genes (15,21). Egr-1 is a crucial regulator of cell proliferation, differentiation, and survival after induction by several stimuli such as growth factors, cytokines, radiation, apoptosis-promoting factors, injury, and stretch (4,15,27). Furthermore, depending on the stimulus and cell type, various signal transduction pathways induce Egr-1, including those mediated by the mitogen-activated protein kinases extracellular signal-regulated kinase 1/2, protein kinase C-␤, Rho GTPase, or p38/c-Jun NH 2 -terminal kinase (8).…”

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confidence: 99%

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RAGE: developmental expression and positive feedback regulation by Egr-1 during cigarette smoke exposure in pulmonary epithelial cells

Reynolds¹,

Kasteler²,

Cosio³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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The receptor for advanced glycation end-products (RAGE) is a member of the immunoglobin superfamily of multiligand receptors. Following ligand binding, mechanisms associated with host defense, tissue remodeling, and inflammation are activated. RAGE is highly expressed in pulmonary epithelium transitioning from alveolar type (AT) II to ATI cells and is upregulated in the presence of ligand; however, the regulation and function of RAGE during development are less clear. Herein, immunohistochemistry demonstrated a temporal-spatial pattern of RAGE expression in pulmonary epithelial cells from embryonic day 17.5 to postnatal day 10. Cotransfection experiments revealed that the mouse RAGE promoter was activated by early growth response gene 1 (Egr-1) and inhibited by thyroid transcription factor-1 (TTF-1) via interaction with specific regulatory elements. A rat ATI cell line (R3/1) with endogenous RAGE expression also differentially regulated RAGE when transfected with TTF-1 or Egr-1. Because Egr-1 is markedly induced in pulmonary epithelial cells exposed to cigarette smoke extract (CSE; Reynolds PR, Hoidal JR. Am J Respir Cell Mol Biol 35: 314 -319, 2006.), we sought to investigate RAGE induction by CSE. Employing RT-PCR and Western blotting, RAGE and common ligands (amphoterin and S100A12) were upregulated in epithelial (R3/1 and A549) and macrophage (RAW) cell lines following exposure to CSE. Immunostaining for RAGE in cells similarly exposed and in lungs from mice exposed to cigarette smoke for 6 mo revealed elevated RAGE expression in pulmonary epithelium. After the addition of glyoxylated BSA, an advanced glycation end-product that binds RAGE, real-time RT-PCR detected a 200-fold increase in Egr-1. These results indicate that Egr-1 regulates RAGE expression during development and the likelihood of positive feedback involving Egr-1 and RAGE in cigarette smokerelated disease.

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confidence: 99%

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confidence: 99%

RAGE: developmental expression and positive feedback regulation by Egr-1 during cigarette smoke exposure in pulmonary epithelial cells

Reynolds¹,

Kasteler²,

Cosio³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It also generates oxidative stress and induces the synthesis and secretion of proinflammatory cytokines and chemotaxis (9). Multiple studies have demonstrated that the AGE-RAGE interaction is involved in such disorders as diabetes (10), rheumatoid arthritis (11), and Sjögren's syndrome (12), suggesting that cellsurface binding of RAGE by AGE may be critically involved in inflammatory responses and may trigger chronic diseases. On the basis of ample published evidence, we hypothesized that RAGE might be important in mediating periapical periodontitis.…”

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Involvement of Inducible Nitric Oxide Synthase and Receptor for Advanced Glycation End Products in Periapical Granulomas

Hama

Takeichi

Ito

2007

Journal of Endodontics

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“…A unique receptor of the immunoglobulin superfamily of cell surface molecules known as the receptor for advanced glycation end products (RAGE) has been implicated in chronic inflammatory conditions such as Sjögren's syndrome, diabetes, and rheumatoid arthritis [1][2][3] . RAGE signaling stimulates a host of pro-inflammatory events.…”

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confidence: 99%

Receptor for Advanced Glycation End Products is Required for HMGB1/S100A4/NF-κβ Interaction In Porphyromonas gingivalis Induced Gingival Inflammation

Sun

Bhawal

et al. 2014

J. Hard Tissue Biology.

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High-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE) are thought to play key roles in the progression of chronic inflammatory diseases. We recently showed that HMGB1 and RAGE might be involved in the progression of human gingival inflammation as novel inflammatory mediators. The molecular mechanisms governing the ability of RAGE to induce ligand-specific responses in gingival inflammation are still unknown. We identified HMGB1/S100A4/NF-κβ pathway, a global regulator of inflammation, as a major RAGE-responsive molecule induced by Porphyromonas gingivalis (P. gingivalis) in rat gingiva. Consistent with the observation that RAGE can be activated by multiple ligands, the elevated expression of RAGE-mediated HMGB1 and S100A4 expression in gingival inflammation. Phosphorylation of NF-κβ and IL-1β immunoreactivity was stronger in P. gingivalis challenged gingiva compared to the control. Quantitative real-time RT-PCR confirmed the increased expression of HMGB1, RAGE, and IL-1β mRNA in P. gingivalis challenged gingiva. Our results indicate that RAGE is a major target gene shared by HMGB1 and S100A4 and the coordinated action of RAGE and NF-κβ leads to the induction of gingival inflammation.

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Receptor of advanced glycation end product (RAGE) expression in the minor salivary glands of patients with Sjo˝gren's syndrome: a preliminary study

Abstract: RAGE is present in the labial salivary glands of both normal and SS patients, with preliminary data suggesting over-expression in SS tissues. The role of RAGE in the pathogenesis of SS has yet to be determined.

Cited by 24 publications

References 16 publications

RAGE: developmental expression and positive feedback regulation by Egr-1 during cigarette smoke exposure in pulmonary epithelial cells

RAGE: developmental expression and positive feedback regulation by Egr-1 during cigarette smoke exposure in pulmonary epithelial cells

Involvement of Inducible Nitric Oxide Synthase and Receptor for Advanced Glycation End Products in Periapical Granulomas

Receptor for Advanced Glycation End Products is Required for HMGB1/S100A4/NF-κβ Interaction In Porphyromonas gingivalis Induced Gingival Inflammation

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