Preventative Effects of 4,4'-Diphenylmethane-bis(methyl) Carbamate Isolated from Cortex Mori on Human Umbilical Vein Endothelial Cell Dysfunction Induced by Advanced Glycation End Products

2011 ◽  
Vol 26 (3) ◽  
pp. 412-419 ◽  
Author(s):  
Liang Feng ◽  
You-hua Xu ◽  
Shan-shan Wang ◽  
Wai Au-yeung ◽  
Zhao-guang Zheng ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Advanced Glycation End Products ◽  
Umbilical Vein ◽  
Endothelial Cell Dysfunction ◽  
Advanced Glycation ◽  
Human Umbilical Vein ◽  
Cell Dysfunction ◽  
Glycation End Products ◽  
End Products ◽  
Cortex Mori

Advanced glycation end products of human β2 glycoprotein I modulate the maturation and function of DCs

Blood ◽  
2011 ◽  
Vol 117 (23) ◽  
pp. 6152-6161 ◽  
Author(s):  
Brigitta Buttari ◽  
Elisabetta Profumo ◽  
Antonella Capozzi ◽  
Francesco Facchiano ◽  
Luciano Saso ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Advanced Glycation End Products ◽  
Target Antigen ◽  
Endothelial Cell Dysfunction ◽  
Advanced Glycation ◽  
Cell Dysfunction ◽  
Glycoprotein I ◽  
Glycation End Products ◽  
End Products ◽  
Chronic Disorders

Abstract In chronic disorders related to endothelial cell dysfunction, plasma β2 glycoprotein I (β2GPI) plays a role as a target antigen of pathogenetic autoimmune responses. However, information is still lacking to clarify why β2GPI triggers autoimmunity. It is possible that posttranslational modification of the protein, such as nonenzymatic glycosylation, leads to the formation of advanced glycation end products (AGEs). The aim of our study was to explore whether glucose-modified β2GPI is able to interact and activate monocyte-derived immature dendritic cells (iDCs) from healthy human donors. SDS-PAGE and spectrofluorometric analyses indicated that β2GPI incubated with glucose was sugar modified, and that this modification likely consisted of AGE formation, resulting in AGE-β2GPI. AGE-β2GPI caused phenotypical and functional maturation of iDCs involving the activation of p38 MAPK, ERK, and NF-κB. It also induced on DCs a significant up-regulation of RAGE, the receptor for AGEs. Evidence for RAGE involvement comes from blocking experiments with an anti-RAGE mAb, confocal analysis, and coimmunoprecipitation experiments. AGE-β2GPI–stimulated DCs had increased allostimulatory ability and primed naive T lymphocytes toward a Th2 polarization. These findings might explain in part the interactive role of β2GPI, AGEs, and DCs in chronic disorders related to endothelial cell dysfunction.

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