Identification of the receptor for advanced glycation end products in synovial tissue of patients with rheumatoid arthritis

Drinda, Stefan; Franke, Sybille; Rüster, Michael; Petrow, Peter; Pullig, Oliver; Stein, Günter; Hein, Gert

doi:10.1007/s00296-004-0456-y

Cited by 58 publications

(38 citation statements)

References 16 publications

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“…SAA, particularly when HDL levels are reduced, may contribute to this process. Because RAGEpositive macrophages and T cells are found in RA synovial tissue (63), and SAA is produced by macrophages and fibroblasts in inflammatory lesions, SAA-RAGE interactions may contribute to localized pathogenesis by directly contributing to fibrin deposition and thrombosis in inflammatory states.…”

Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

106

121

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C-reactive protein (CRP) and serum amyloid A (SAA) increase in the blood of patients with inflammatory conditions and CRP-induced monocyte tissue factor (TF) may contribute to inflammation-associated thrombosis. This study demonstrates that SAA is a potent and rapid inducer of human monocyte TF. SAA induced TF mRNA in PBMC within 30 min and optimal procoagulant activity within 4 h, whereas CRP (25 μg/ml)-induced activity was minimal at this time. Unlike CRP, SAA did not synergize with LPS. Procoagulant activity was inhibited by anti-TF and was dependent on factors VII and X, and TF Ag levels were elevated on CD14+ monocytes. Responses were optimal with lymphocytes, although these were not obligatory. Inhibitor studies indicate activation of NF-κB through the ERK1/2 and p38 MAPK pathways; the cyclo-oxygenase pathway was not involved. SAA-induced TF was partially inhibited by high-density lipoprotein, but not by low-density lipoprotein or by apolipoprotein A-I. SAA is a ligand for the receptor for advanced glycation end products (RAGE), and TF generation was suppressed by ∼50% by a RAGE competitor, soluble RAGE, and by ∼85% by anti-RAGE IgG. However, another RAGE ligand, high mobility group box-1 protein, capable of inducing monocyte chemotactic protein-1 mRNA in 2 h, did not induce TF within 24 h. Cross-linking studies confirmed SAA binding to soluble RAGE. Elevated SAA is a marker of disease activity in patients with rheumatoid arthritis, and PBMC from patients with rheumatoid arthritis were more sensitive to SAA than normals, suggesting a new link between inflammation and thrombosis.

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Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

106

121

View full text Add to dashboard Cite

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“…Increased RAGE levels have been detected in the synovial tissues of patients with inflammatory joint diseases (7). AGE/RAGE interactions stimulate the release of inflammatory cytokines such as IL-1, IL-2, and TNF-α (6,15).…”

Section: Discussionmentioning

confidence: 99%

“…Thay are expressed on multiple cell types such as endothelial cells, neutrophils, macrophages, monocytes, lymphocytes (T and B cells), fibroblasts, and neurons (5,7,9,14,10). Apoptotic smooth muscle cells and macrophages associated with atherosclerotic plaques were shown to have increased levels of RAGE; especially in those of diabetic patients (3).…”

Section: Introductionmentioning

confidence: 99%

RAGE mRNA Expression and Its Correlation with Nuclear Factor Kappa Beta mRNA Expression in Inflamed Human Periradicular Tissues

Crabtree

Pileggi

Bhattacharyya

et al. 2008

Journal of Endodontics

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Advanced glycation end-products (AGEs) have been found to play a role in inflammation and vascular complications. The receptor for AGE (RAGE) is expressed on many cells and is upregulated during inflammation. To date, RAGE expression or its correlation with NF-kβ expression has not been demonstrated in inflammatory periapical lesions. In this study, periapical tissue was obtained from 38 patients and processed for RAGE and NF-kβ expression using RT-PCR. Various patient variables were examined as predictors for these novel proteins expressions. The results demonstrated a statistically significant positive correlation between the expression of RAGE and NF-kβ (p=0.001). When comparing Caucasians and African-Americans, a statistically significant difference was noted with the African-American group showing a higher expression of RAGE (ANOVA F= 12.746, p=0.002). In conclusion, a positive linear correlation of their presence was demonstrated in inflamed periradicular tissues. This study outlines the possible use of these proteins as potential markers for periapical inflammation.

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“…Advanced glycation end products (AGEs), which are formed during the Maillard reaction by non-enzymatic glycation, and oxidation of proteins were detected in the synovial lining, sublining, and endothelium in RA patiens. CML showed positive immunostaining in some RA macrophages (CD68+) and T cells (CD45RO+) (Drinda et al, 2002). High levels of protein carbonyl (PCO), and AGE products were found in serum of collagen -induced arthritis mice (Choi, 2007).…”

Section: Markers Of Oxidative Stress In Human Autoimmune Joint Diseasesmentioning

confidence: 99%

Oxidative Stress in Human Autoimmune Joint Diseases

Škurlová¹

2012

Oxidative Stress and Diseases

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Identification of the receptor for advanced glycation end products in synovial tissue of patients with rheumatoid arthritis

Abstract: We detected RAGE in RA and OA synovial tissue. The presence of RAGE on macrophages, T cells, and some B cells suggests its role in the pathogenesis of inflammatory joint disease.

Cited by 58 publications

References 16 publications

Serum Amyloid A Induces Monocyte Tissue Factor

Serum Amyloid A Induces Monocyte Tissue Factor

RAGE mRNA Expression and Its Correlation with Nuclear Factor Kappa Beta mRNA Expression in Inflamed Human Periradicular Tissues

Oxidative Stress in Human Autoimmune Joint Diseases

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