scholarly journals Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Cheng-Hsien Chen ◽  
Tso-Hsiao Chen ◽  
Mei-Yi Wu ◽  
Tz-Chong Chou ◽  
Jia-Rung Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Advanced Glycation End Products ◽  
Vascular Endothelial Cells ◽  
Far Infrared ◽  
Vascular Endothelial ◽  
Diabetic Mice ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals RasGRP2 inhibits glyceraldehyde-derived toxic advanced glycation end-products from inducing permeability in vascular endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jun-ichi Takino ◽  
Takuma Sato ◽  
Takumi Kanetaka ◽  
Kasumi Okihara ◽  
Kentaro Nagamine ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Permeability ◽  
Advanced Glycation End Products ◽  
Protective Factor ◽  
Vascular Endothelial Cells ◽  
Enzymatic Reaction ◽  
Vascular Endothelial ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

AbstractAdvanced glycation end-products (AGEs) are formed by the non-enzymatic reaction of sugars and proteins. Among the AGEs, glyceraldehyde-derived toxic AGEs (TAGE) are associated with various diseases, including diabetic complications such as diabetic retinopathy (DR). The risk of developing DR is strongly associated with poor glycemic control, which causes AGE accumulation and increases AGE-induced vascular permeability. We previously reported that Ras guanyl nucleotide releasing protein 2 (RasGRP2), which activates small G proteins, may play an essential role in the cell response to toxicity when exposed to various factors. However, it is not known whether RasGRP2 prevents the adverse effects of TAGE in vascular endothelial cells. This study observed that TAGE enhanced vascular permeability by disrupting adherens junctions and tight junctions via complex signaling, such as ROS and non-ROS pathways. In particular, RasGRP2 protected adherens junction disruption, thereby suppressing vascular hyper-permeability. These results indicate that RasGRP2 is an essential protective factor of vascular permeability and may help develop novel therapeutic strategies for AGE-induced DR.

scholarly journals Novel splice variants of the receptor for advanced glycation end-products expressed in human vascular endothelial cells and pericytes, and their putative roles in diabetes-induced vascular injury

2003 ◽  
Vol 370 (3) ◽  
pp. 1097-1109 ◽  
Author(s):  
Hideto YONEKURA ◽  
Yasuhiko YAMAMOTO ◽  
Shigeru SAKURAI ◽  
Ralica G. PETROVA ◽  
Md. Joynal ABEDIN ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Advanced Glycation End Products ◽  
Splice Variants ◽  
Vascular Complications ◽  
Full Length ◽  
Vascular Endothelial ◽  
Advanced Glycation ◽  
Diabetic Vascular Complications ◽  
Glycation End Products ◽  
End Products

The binding of advanced glycation end-products (AGE) to the receptor for AGE (RAGE) is known to deteriorate various cell functions and is implicated in the pathogenesis of diabetic vascular complications. In the present study, we show that the cellular constituents of small vessels, endothelial cells (EC) and pericytes express novel splice variants of RAGE mRNA coding for the isoforms that lack the N-terminal V-type immunoglobulin-like domain (N-truncated) or the C-terminal transmembrane domain (C-truncated), as well as the known full-length mRNA. The ratio of the expression of the three variants was different between EC and pericytes; the content of the C-truncated form was highest in EC, whereas the full-length form was the most abundant in pericytes. Transfection experiments with COS-7 cells demonstrated that those variant mRNAs were translated into proteins as deduced; C-truncated RAGE was efficiently secreted into the culture media, and N-truncated RAGE was located mainly on the plasma membrane. The three isoforms were also detected in primary cultured human EC and pericytes. Further, full-length and C-truncated forms of RAGE bound to an AGE-conjugated column, whereas N-truncated RAGE did not. The AGE induction of extracellular-signal-related kinase phosphorylation and vascular endothelial growth factor in EC and of the growth and cord-like structure formation of EC was abolished completely by C-truncated RAGE, indicating that this endogenous secretory receptor (endogenous secretory RAGE) is cytoprotective against AGE. The results may contribute to our understanding of the molecular basis for the diversity of cellular responses to AGE and for individual variations in the susceptibility to diabetic vascular complications.

Sign in / Sign up

Export Citation Format

Share Document