scholarly journals Endocytic uptake of advanced glycation end products by mouse liver sinusoidal endothelial cells is mediated by a scavenger receptor distinct from the macrophage scavenger receptor class A

2000 ◽  
Vol 352 (1) ◽  
pp. 233 ◽  
Author(s):  
Kenshi MATSUMOTO ◽  
Hiroyuki SANO ◽  
Ryoji NAGAI ◽  
Hiroshi SUZUKI ◽  
Tatsuhiko KODAMA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mouse Liver ◽  
Scavenger Receptor ◽  
Advanced Glycation ◽  
Liver Sinusoidal Endothelial Cells ◽  
Class A ◽  
Macrophage Scavenger Receptor ◽  
Scavenger Receptor Class ◽  
Glycation End Products ◽  
End Products

scholarly journals Endocytic uptake of advanced glycation end products by mouse liver sinusoidal endothelial cells is mediated by a scavenger receptor distinct from the macrophage scavenger receptor class A

2000 ◽  
Vol 352 (1) ◽  
pp. 233-240 ◽  
Author(s):  
Kenshi MATSUMOTO ◽  
Hiroyuki SANO ◽  
Ryoji NAGAI ◽  
Hiroshi SUZUKI ◽  
Tatsuhiko KODAMA ◽  
...  
Keyword(s):  
Scavenger Receptor ◽  
Peritoneal Macrophages ◽  
Wild Type ◽  
Advanced Glycation ◽  
Liver Sinusoidal Endothelial Cells ◽  
Knock Out ◽  
Class A ◽  
Macrophage Scavenger Receptor ◽  
Scavenger Receptor Class ◽  
Glycation End Products

Previous studies with peritoneal macrophages obtained from macrophage scavenger receptor class A (MSR-A) knock-out mice showed that the endocytic uptake of advanced glycation end products (AGE) by macrophages was mediated mainly by MSR-A. However, it is controversial whether the endocytic uptake of intravenously injected AGE proteins by liver sinusoidal endothelial cells (LECs) is similarly explained by receptor-mediated endocytosis via MSR-A. The present study was conducted to compare the capacity to endocytose AGE proteins in LECs and peritoneal macrophages obtained from MSR-A knock-out and littermate wild-type mice. The endocytic degradation capacity of MSR-A knock-out LECs for AGE–BSA was indistinguishable from that of wild-type LECs, whereas that of MSR-A knock-out peritoneal macrophages for AGE–BSA was decreased to 30% of that in wild-type cells. Similarly, the endocytic degradation of MSR-A knock-out LECs for acetylated low-density lipoprotein (acetyl-LDL) did not differ from that of wild-type LECs, whereas the endocytic degradation of acetyl-LDL by MSR-A knock-out peritoneal macrophages was less than 20% of that in wild-type cells. Furthermore, formaldehyde-treated serum albumin (f-Alb), a ligand known to undergo scavenger-receptor-mediated endocytosis by LECs, was effectively taken up by MSR-A knock-out LECs at a capacity that did not differ from that of wild-type LECs. Moreover, the endocytic uptake of AGE–BSA by LECs was effectively competed for by unlabelled f-Alb or acetyl-LDL. These results indicate that the scavenger-receptor ligands AGE proteins, acetyl-LDL and f-Alb are endocytosed by LECs through a non-MSR-A pathway.

scholarly journals A comparative study of sulphated polysaccharide effects on advanced glycation end-product uptake and scavenger receptor class A level in macrophages

2020 ◽  
Vol 17 (1) ◽  
pp. 147916411989697 ◽  
Author(s):  
Takashi Nishinaka ◽  
Shuji Mori ◽  
Yui Yamazaki ◽  
Atsuko Niwa ◽  
Hidenori Wake ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Chondroitin Sulphate ◽  
Scavenger Receptor ◽  
Dextran Sulphate ◽  
Advanced Glycation ◽  
Sulphated Polysaccharides ◽  
Advanced Glycation End Product ◽  
Class A ◽  
Glycation End Products ◽  
End Products

Advanced glycation end-products, especially toxic advanced glycation end-products derived from glyceraldehyde (advanced glycation end-product-2) and glycolaldehyde (advanced glycation end-product-3), are biologically reactive compounds associated with diabetic complications. We previously demonstrated that toxic advanced glycation end-products were internalised into macrophage-like RAW264.7 cells through scavenger receptor-1 class A (CD204). Toxic advanced glycation end-product uptake was inhibited by fucoidan, a sulphated polysaccharide and antagonistic ligand for scavenger receptors, suggesting that sulphated polysaccharides are emerging candidates for treatment of advanced glycation end-product–related diseases. In this study, we compared the effects of six types of sulphated and non-sulphated polysaccharides on toxic advanced glycation end-product uptake in RAW264.7 cells. Fucoidan, carrageenan and dextran sulphate attenuated toxic advanced glycation end-product uptake. Fucoidan and carrageenan inhibited advanced glycation end-product-2–induced upregulation of SR-A, while advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A was only suppressed by fucoidan. Dextran sulphate did not affect scavenger receptor-1 class A levels in toxic advanced glycation end-product–treated cells. Chondroitin sulphate, heparin and hyaluronic acid failed to attenuate toxic advanced glycation end-product uptake. Heparin and hyaluronic acid had no effect on scavenger receptor-1 class A levels, while chondroitin sulphate inhibited advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A. Taken together, fucoidan and carrageenan, but not the other sulphated polysaccharides examined, had inhibitory activities on toxic advanced glycation end-product uptake and toxic advanced glycation end-product–induced upregulation of scavenger receptor-1 class A, possibly because of structural differences among sulphated polysaccharides.

scholarly journals Insulin Enhances Macrophage Scavenger Receptor-mediated Endocytic Uptake of Advanced Glycation End Products

1998 ◽  
Vol 273 (15) ◽  
pp. 8630-8637 ◽  
Author(s):  
Hiroyuki Sano ◽  
Takayuki Higashi ◽  
Kenshi Matsumoto ◽  
Jukka Melkko ◽  
Yoshiteru Jinnouchi ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Scavenger Receptor ◽  
Advanced Glycation ◽  
Macrophage Scavenger Receptor ◽  
Glycation End Products ◽  
End Products
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