scholarly journals Diesel Particulate Matter Induces Receptor for Advanced Glycation End‐Products (RAGE) Expression in Alveolar Epithelial Cells and Mediates an Inflammatory Response

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Karisa M Wasley ◽  
Camille H Allison ◽  
Paul R Reynolds
Keyword(s):  
Particulate Matter ◽  
Inflammatory Response ◽  
Alveolar Epithelial Cells ◽  
Diesel Particulate Matter ◽  
Advanced Glycation ◽  
Diesel Particulate ◽  
Alveolar Epithelial ◽  
Glycation End Products ◽  
End Products ◽  
Rage Expression

scholarly journals Reduced receptor for advanced glycation end products is associated with α-SMA expression in patients with idiopathic pulmonary fibrosis and mice

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Hyosin Baek ◽  
Soojin Jang ◽  
Jaehyun Park ◽  
Jimin Jang ◽  
Jooyeon Lee ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Western Blot ◽  
Advanced Glycation End Products ◽  
Alveolar Epithelial Cells ◽  
Advanced Glycation ◽  
Alveolar Epithelial ◽  
Glycation End Products ◽  
End Products ◽  
Rage Expression

Abstract Background Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease. Despite alveolar epithelial cells is crucial role in lung, its contribution and the associated biomarker remain unknown in the pathogenesis of IPF. Recently, environmental factors including stone dust, silica and cigarette smoking were found as risk factors involved in IPF. Receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin super family of cell surface receptors. It has been shown that interaction between RAGE and its ligands on immune cells mediates cellular migration and regulation of pro-inflammation. RAGE is highly expressed in the lung, in particular, alveolar epithelial cells. Therefore, we determined whether RAGE expression is associated with fibrosis-associated genes in patients with IPF and mice. Results When bleomycin (BLM) was intratracheally administered to C57BL/6 mice for 1, 2 weeks, macrophage and neutrophils were significantly increased. The fibrotic nodule formed and accumulation of collagen was determined after BLM injection in H&E- and Masson’s trichrome staining. Levels of elastin, Col1a1 and fibronectin were increased in quantitative real-time PCR and protein levels of α-SMA was increased in western blot analysis. In the lung tissues of 1 mg/kg BLM-induced mice, RAGE expression was gradually decreased in 1- and 2 weeks in immunohistochemistry and western blot analysis, and 3 mg/kg of BLM-induced mice exhibited decreased RAGE levels while α-SMA expression was increased. We next determined RAGE expression in the lungs of IPF patients using immunohistochemistry. As a result, RAGE expression was decreased, while α-SMA expression was increased compared with non-IPF subjects. Conclusions Our findings suggest that reduced RAGE was associated with increased fibrotic genes in BLM-induced mice and patients with IPF. Therefore, RAGE could be applied with a biomarker for prognosis and diagnosis in the pathogenesis of IPF.

scholarly journals Proteolytic release of the receptor for advanced glycation end products from in vitro and in situ alveolar epithelial cells

2011 ◽  
Vol 300 (4) ◽  
pp. L516-L525 ◽  
Author(s):  
Naoko Yamakawa ◽  
Tokujiro Uchida ◽  
Michael A. Matthay ◽  
Koshi Makita
Keyword(s):  
Epithelial Cells ◽  
Advanced Glycation End Products ◽  
Alveolar Epithelial Cells ◽  
Advanced Glycation ◽  
Alveolar Epithelial ◽  
Lps Challenge ◽  
Soluble Rage ◽  
Glycation End Products ◽  
End Products

Although the receptor for advanced glycation end products (RAGE) has been used as a biological marker of alveolar epithelial cell injury in clinical studies, the mechanism for release of soluble RAGE from lung epithelial cells has not been well studied. Therefore, these studies were designed to determine the mechanism for release of soluble RAGE after lipopolysaccharide (LPS) challenge. For these purposes, alveolar epithelial cells from rat lungs were cultured on Transwell inserts, and LPS was added to the apical side (500 μg/ml) for 16 h on day 7. On day 7, RAGE was expressed predominantly in surfactant protein D-negative cells, and LPS challenge induced release of RAGE into the medium. This response was partially blocked by matrix metalloproteinase (MMP) inhibitors. Transcripts of MMP-3 and MMP-13 were upregulated by LPS, whereas RAGE transcripts did not change. Proteolysis by MMP-3 and MMP-13 resulted in soluble RAGE expression in the bronchoalveolar lavage fluid in the in situ rat lung, and this reaction was inhibited by MMP inhibitors. In human studies, both MMP-3 and -13 antigen levels were significantly correlated with the level of RAGE in pulmonary edema fluid samples. These results support the conclusion that release of RAGE is primarily mediated by proteolytic damage in alveolar epithelial cells in the lung, caused by proteases in acute inflammatory conditions in the distal air spaces.

scholarly journals Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries

2022 ◽  
Vol 17 (1) ◽  
Author(s):  
Bin-Fei Zhang ◽  
Wei Song ◽  
Jun Wang ◽  
Peng-Fei Wen ◽  
Yu-Min Zhang
Keyword(s):  
Lung Injury ◽  
Western Blot ◽  
High Mobility ◽  
Alveolar Epithelial Cells ◽  
Advanced Glycation ◽  
Jnk Pathway ◽  
Alveolar Epithelial ◽  
Glycation End Products ◽  
End Products ◽  
Crush Injuries

Abstract Objectives The lung injury is often secondary to severe trauma. In the model of crush syndrome, there may be secondary lung injury. We hypothesize that high-mobility group box 1 (HMGB1), released from muscle tissue, mediates the apoptosis of alveolar epithelial cells (AEC) via HMGB1/Receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway. The study aimed to investigate how HMGB1 mediated the apoptosis of AEC in the rat model. Methods Seventy-five SD male rats were randomly divided into five groups: CS, CS + vehicle, CS + Ethyl pyruvate (EP), CS + FPS-ZM1 group, and CS + SP600125 groups. When the rats CS model were completed after 24 h, the rats were sacrificed. We collected the serum and the whole lung tissues. Inflammatory cytokines were measured in serum samples. Western blot and RT-qPCR were used to quantify the protein and mRNA. Lastly, apoptotic cells were detected by TUNEL. We used SPSS 25.0 for statistical analyses. Results Nine rats died during the experiments. Dead rats were excluded from further analysis. Compared to the CS group, levels of HMGB1 and inflammatory cytokines in serum were downregulated in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups. Western blot and RT-qPCR analysis revealed a significant downregulation of HMGB1, RAGE, and phosphorylated-JNK in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups, compared with the CS groups, excluding total-JNK mRNA. Apoptosis of AEC was used TUNEL to assess. We found the TUNEL-positive cells were downregulated in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups. Conclusion The remote lung injury begins early after crush injuries. The HMGB1/RAGE/JNK signaling axis is an attractive target to abrogate the apoptosis of AEC after crush injuries.

Type II Alveolar Epithelial Cells in Lung Express Receptor for Advanced Glycation End Products (RAGE) Gene

1997 ◽  
Vol 238 (2) ◽  
pp. 512-516 ◽  
Author(s):  
Fumiki Katsuoka ◽  
Yasushi Kawakami ◽  
Takeo Arai ◽  
Hiroyuki Imuta ◽  
Masachika Fujiwara ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Advanced Glycation End Products ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Advanced Glycation ◽  
Alveolar Epithelial ◽  
Glycation End Products ◽  
End Products

Blockade of TGF-β-activated kinase 1 prevents advanced glycation end products-induced inflammatory response in macrophages

Cytokine ◽  
2016 ◽  
Vol 78 ◽  
pp. 62-68 ◽  
Author(s):  
Xingxin Xu ◽  
Xiangming Qi ◽  
Yunxia Shao ◽  
Yuanyuan Li ◽  
Xin Fu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

ONO-2506 alleviates lipopolysaccharide-induced hippocampal neuroinflammation and apoptosis

2019 ◽  
Author(s):  
Jian-yu Liu ◽  
Wei Fang ◽  
Shi-xia Cai ◽  
Ming-ying Dai ◽  
Bo Yao
Keyword(s):  
S100 Protein ◽  
Brain Cell ◽  
Potential Treatment ◽  
Advanced Glycation ◽  
High Concentration ◽  
Tnf Α ◽  
Glycation End Products ◽  
End Products ◽  
Neurotoxic Effects ◽  
Rage Expression

Abstract Background Sepsis associated encephalopathy has high mortality rate, but there is no targeted therapy to reduce brain damage in septic patients. In our previous study, we found that S100β concentration was higher in patients with SAE. At high concentration, S100β exerts neurotoxic effects through receptor for advanced glycation end products (RAGE). RAGE-activated signalling could induce the inflammatory response. And neuroinflammation is an important mechanism of SAE. So inhibiting S100β expression may be a potential treatment of SAE. ONO-2506 can inhibit the production and release of S100 protein from astrocytes. In this study, we administered ONO-2506 to mice in order to evaluate its effectiveness on neuroinflammation and apoptosis in hippocampus induced by lipopolysaccharides. Results We found administration with lipopolysaccharides increased the levels of S100β, RAGE, IL-β, TNF-α and the TUNEL positive brain cells in hippocampus tissue. The ONO-2506 30mg/kg and 90mg/kg could reduce the levels of neuroinflammation (IL-β and TNF-α), and alleviate the apoptosis in hippocampus. Conclusions ONO-2506 could reduce the neuroinflammation and alleviate brain cell apoptosis in hippocampus of LPS mice models. Moreover, the RAGE expression was inhibited after ONO-2506 treatment.

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