Advanced glycation end products increase expression of S100A8 and A9viaRAGE-MAPK in rat dental pulp cells

Oral Diseases ◽  
2014 ◽  
Vol 21 (3) ◽  
pp. 328-334 ◽  
Author(s):  
Y Nakajima ◽  
Y Inagaki ◽  
J Kido ◽  
T Nagata

2013 ◽  
Vol 39 (7) ◽  
pp. 873-878 ◽  
Author(s):  
Yukiko Nakajima ◽  
Yuji Inagaki ◽  
Yuka Hiroshima ◽  
Jun-ichi Kido ◽  
Toshihiko Nagata


Oral Diseases ◽  
2021 ◽  
Author(s):  
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Jiro Miura ◽  
Masato Shimizu ◽  
Aoi Takashima ◽  
Yusuke Matsuda ◽  
...  


2015 ◽  
Vol 41 (11) ◽  
pp. 1852-1861 ◽  
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Heinz-Dieter Müller ◽  
Barbara Cvikl ◽  
Klara Janjić ◽  
Sylvia Nürnberger ◽  
Andreas Moritz ◽  
...  


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.







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