scholarly journals EVALUATION OF RECEPTOR FOR ADVANCED GLYCATION END PRODUCT /HIGH-MOBILITY GROUP BOX 1 (RAGE/HMGB1) EXPRESSION STATUS AND ITS PROGNOSTIC VALUE IN BREAST CANCER

2019 ◽  
Vol 37 (1) ◽  
pp. 17-36
2015 ◽  
Vol 15 (1) ◽  
pp. 109-123 ◽  
Author(s):  
Elisa Maurizio ◽  
Jacek R. Wiśniewski ◽  
Yari Ciani ◽  
Angela Amato ◽  
Laura Arnoldo ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Salunya Tancharoen ◽  
Tassanee Tengrungsun ◽  
Theeralaksna Suddhasthira ◽  
Kiyoshi Kikuchi ◽  
Nuttavun Vechvongvan ◽  
...  

High mobility group box 1 (HMGB1), a nonhistone DNA-binding protein, is released into the extracellular space and promotes inflammation. HMGB1 binds to related cell signaling transduction receptors, including receptor for advanced glycation end products (RAGE), which actively participate in vascular and inflammatory diseases. The aim of this study was to examine whether RAGE and HMGB1 are involved in the pathogenesis of pulpitis and investigate the effect of Prevotella intermedia (P. intermedia) lipopolysaccharide (LPS) on RAGE and HMGB1 expression in odontoblast-like cells (OLC-1). RAGE and HMGB1 expression levels in clinically inflamed dental pulp were higher than those in healthy dental pulp. Upregulated expression of RAGE was observed in odontoblasts, stromal pulp fibroblasts-like cells, and endothelial-like cell lining human pulpitis tissue. Strong cytoplasmic HMGB1 immunoreactivity was noted in odontoblasts, whereas nuclear HMGB1 immunoreactivity was seen in stromal pulp fibroblasts-like cells in human pulpitis tissue. LPS stimulated OLC-1 cells produced HMGB1 in a dose-dependent manner through RAGE. HMGB1 translocation towards the cytoplasm and secretion from OLC-1 in response to LPS was inhibited by TPCA-1, an inhibitor of NF-κB activation. These findings suggest that RAGE and HMGB1 play an important role in the pulpal immune response to oral bacterial infection.


2019 ◽  
Vol 316 (1) ◽  
pp. L280-L290 ◽  
Author(s):  
Sisi Chen ◽  
Guangyuan Yu ◽  
Jun Xie ◽  
Wei Tang ◽  
Leiqiong Gao ◽  
...  

The type 2 immune response, induced by infection of respiratory syncytial virus (RSV), has been linked to asthma development, but it remains unclear how the response is initiated. Here, we reported that the high-mobility group box-1 (HMGB1) protein promotes the type 2 response in the later stage of RSV infection. In mice, we found that type 2 cytokines were elevated in the later stages, which were strongly diminished after administration of anti-HMGB1 antibodies. Further investigation revealed that HMGB1 expression was localized to CC10+ club cells in the lung. In the clinic, levels of HMGB1 in nasopharyngeal aspirates in hospitalized infants with RSV bronchiolitis [median (interquartile range) 161.20 ng/ml (68.06–221.30)] were significantly higher than those without lower respiratory tract infections [21.94 ng/ml (12.12–59.82); P < 0.001]. Moreover, higher levels of HMGB1 correlated with clinical severity. These results reveal a link between viral infection and the asthma-like type 2 responses that are associated with long-term consequences.


2021 ◽  
Vol 22 (20) ◽  
pp. 11276
Author(s):  
Fabian Essig ◽  
Lilith Babilon ◽  
Christoph Vollmuth ◽  
Alexander M. Kollikowski ◽  
Mirko Pham ◽  
...  

High-mobility group box 1 protein (HMGB1) is a damage-associated molecular pattern (DAMP) involved in neutrophil extracellular trap (NET) formation and thrombosis. NETs are regularly found in cerebral thromboemboli. We here analyzed associated HMGB1 expression in human thromboemboli retrieved via mechanical thrombectomy from 37 stroke patients with large vessel occlusion. HMGB1 was detected in all thromboemboli, accounting for 1.7% (IQR 0.6–6.2%) of the total thromboemboli area and was found to be colocalized with neutrophils and NETs and in spatial proximity to platelets. Correlation analysis revealed that the detection of HMGB1 was strongly related to the number of neutrophils (r = 0.58, p = 0.0002) and platelets (r = 0.51, p = 0.001). Our results demonstrate that HMGB1 is a substantial constituent of thromboemboli causing large vessel occlusion stroke.


2019 ◽  
Vol 179 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Mikhail Gorbounov ◽  
Neil M. Carleton ◽  
Rebecca J. Asch-Kendrick ◽  
Lingling Xian ◽  
Lisa Rooper ◽  
...  

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