Receptor for Advanced Glycation End Product (RAGE) Upregulation in Human Gingival Fibroblasts Incubated With Nornicotine

Katz, Joseph; Caudle, Robert M.; Bhattacharyya, Indraneel; Stewart, Carol M.; Cohen, Donald M.

doi:10.1902/jop.2005.76.7.1171

Cited by 81 publications

(99 citation statements)

References 29 publications

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“…7,16,19,20 Moreover, tobacco smoking increases the AGES-RAGE interactions thereby increasing the production of destructive inflammatory cytokines, such as IL-6 and IL-1b. 10,11 Increased levels of these cytokines in the oral fluids have been associated with the etiology of periodontal and peri-implant diseases. [21][22][23] Interestingly, our results showed no statistically significant difference in peri-implant PD, BOP, PI, and mesial and distal CBL around short implants placed in both groups.…”

Section: Discussionmentioning

confidence: 99%

Comparison of peri‐implant clinical and radiographic status around short (6 mm in length) dental implants placed in cigarette‐smokers and never‐smokers: Six‐year follow‐up results

Abduljabbar

Al-Hamoudi

Al-Sowygh

et al. 2017

Clin Implant Dent Rel Res

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Background: It is hypothesized that peri-implant clinical and radiographic inflammatory parameters (probing depth [PD], bleeding on probing [BOP] and plaque index [PI]; and radiographic (crestal bone loss [CBL]) are worse among cigarette-smokers (CS) compared with never-smokers (NS) with short implants.Purpose: The present 6-year follow-up retrospective study compared the peri-implant clinical and radiographic parameters in CS and NS with short dental implants (6 mm in length). Materials and methods:Fifty-six male individuals were included. These individuals divided into 2 groups as follows: (a) Group-1: 29 self-reported systemically healthy CS with 48 short-implants; and (b) Group-2: 27 self-reported systemically healthy NS with 43 short implants. Peri-implant PD, PI, BOP, and CBL were measured. Group comparisons were done using the Kruskal-Wallis test and sample size was estimated. Level of significance was set at P values < .05. Results:In groups 1 and 2, the follow-up durations were 6.2 6 0.1 years and 6.1 6 0.3 years, respectively. A cigarette smoking history of 8.9 6 3.6 pack years was reported by individuals in Group-1. At follow-up, scores of peri-implant PD, BOP, PI, and mesial and distal CBL were comparable around short implants in both groups. Conclusion:Under strict oral hygiene maintenance protocols, short dental implants can remain functionally stable in CS in a manner similar to NS.

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Section: Discussionmentioning

confidence: 99%

Comparison of peri‐implant clinical and radiographic status around short (6 mm in length) dental implants placed in cigarette‐smokers and never‐smokers: Six‐year follow‐up results

Abduljabbar

Al-Hamoudi

Al-Sowygh

et al. 2017

Clin Implant Dent Rel Res

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“…Interestingly, incubation with nornicotine has recently been shown to induce RAGE upregulation in human gingival fibroblasts, involving RAGE in smoke-related periodontal disease. 32 Further studies are needed to clarify the association of RAGE with smoking and airway damage. RAGE-ligand expression in non-neoplastic lung diseases P Morbini et al sRAGE is a secreted form of the receptor produced by alternative splicing of RAGE mRNA and is present in serum and alveolar exudate.…”

Section: Discussionmentioning

confidence: 99%

The receptor for advanced glycation end products and its ligands: a new inflammatory pathway in lung disease?

et al. 2006

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The binding of the receptor for advanced glycation end products (RAGE) with its ligands begins a sustained period of cellular activation and inflammatory signal amplification in different tissues and diseases. This binding could represent an as yet uninvestigated pathway of inflammatory reaction in the lung, where the presence of the receptor has been largely documented and advanced glycation end products (AGEs) are produced by nonenzymatic glycation and oxidation of proteins and lipids, driven by smoke and pollutants exposure or inflammatory stress. We immunohistochemically assessed the expression of RAGE and of its major proinflammatory ligands, N-e-carboxy-methyl-lysine, S100B and S-100A12 in normal lung and in nonneoplastic lung disorders including smoke-related airway disease, granulomatous inflammation, postobstructive damage and usual interstitial pneumonia. In normal lung low expression of the receptor was observed in bronchiolar epithelia, type II pneumocytes, macrophages and some endothelia. S100A12 and S100B were expressed, respectively, in granulocytes and in dendritic cells. Carboxy-methyl-lysine was present in bronchiolar epithelia and macrophages. In all pathological conditions associated with inflammation and lung damage overexpression of both the receptor and of AGEs was observed in bronchiolar epithelia, type II alveolar pneumocytes, alveolar macrophages and endothelia. RAGE overexpression was more evident in epithelia associated with inflammatory cell aggregates. Fibroblasts in usual interstitial pneumonia expressed both the receptor and AGEs. The number of S100A12 and S100B immunoreactive inflammatory cells was variable. S100A12 was also expressed in mononuclear inflammatory cells and in activated epithelia. The activation of the inflammatory pathway controlled by the RAGE is not specific of a single lung disease, however, it may be relevant as a nonspecific pathway of sustained inflammation in lung tissue, and on this basis therapeutic approaches based on receptor blockage can be envisaged.

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“…As an inflammation amplification factor, RAGE expression was found increasing during inflammation (23,(43)(44)(45)(46). To test whether RAGE plays a role in intestinal inflammation, we examined RAGE expression in intestinal epithelial monolayers treated with or without proinflammatory cytokines.…”

Section: The Expression Of Rage Is Up-regulated Under Inflammatory Comentioning

confidence: 99%

Receptor for Advanced Glycation Endproducts Mediates Neutrophil Migration across Intestinal Epithelium

Zen

Chen

et al. 2007

The Journal of Immunology

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Receptor for advanced glycation endproducts (RAGE) is an Ig superfamily cell surface receptor that interacts with a diverse array of ligands associated with inflammatory responses. In this study, we provide evidence demonstrating that RAGE is involved in inflammatory responses in the intestines. We showed that RAGE is expressed in intestinal epithelial cells, primarily concentrated at the lateral membranes close to the apical cell junction complexes. Although RAGE expression was low in epithelium under normal conditions, this protein was up-regulated after treatment with the inflammatory cytokines IFN-γ and/or TNF-α. RAGE expression was also elevated in colon tissue samples from patients with inflammatory bowel diseases. Using in vitro transmigration assays, we found that RAGE mediates neutrophil (polymorphonuclear leukocytes (PMN)) adhesion to, and subsequent migration across, intestinal epithelial monolayers. This activity appears to be mediated by the binding of RAGE to the PMN-specific β2 integrin CD11b/CD18. Thus, these results provide a novel mechanism for the regulation of PMN transepithelial migration and may suggest a new therapeutic target for intestinal inflammation.

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Receptor for Advanced Glycation End Product (RAGE) Upregulation in Human Gingival Fibroblasts Incubated With Nornicotine

Abstract: Nornicotine, AGE, and upregulation of RAGE may be involved in the pathogenesis of periodontal disease associated with smoking.

Cited by 81 publications

References 29 publications

Comparison of peri‐implant clinical and radiographic status around short (6 mm in length) dental implants placed in cigarette‐smokers and never‐smokers: Six‐year follow‐up results

Comparison of peri‐implant clinical and radiographic status around short (6 mm in length) dental implants placed in cigarette‐smokers and never‐smokers: Six‐year follow‐up results

The receptor for advanced glycation end products and its ligands: a new inflammatory pathway in lung disease?

Receptor for Advanced Glycation Endproducts Mediates Neutrophil Migration across Intestinal Epithelium

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