scholarly journals Neuronal cell death and regeneration in diseases associated with advanced glycation end-products accumulation

2014 ◽  
Vol 9 (7) ◽  
pp. 701 ◽  
Author(s):  
Toshiyuki Oshitari ◽  
Shuichi Yamamoto ◽  
Guzel Bikbova
Keyword(s):  
Cell Death ◽  
Advanced Glycation End Products ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Suppression of Hepatic Stellate Cell Death by Toxic Advanced Glycation End-Products

2021 ◽  
Vol 44 (1) ◽  
pp. 112-117
Author(s):  
Jun-ichi Takino ◽  
Takuma Sato ◽  
Kentaro Nagamine ◽  
Akiko Sakasai-Sakai ◽  
Masayoshi Takeuchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Advanced Glycation End Products ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Advanced Glycation End Products Mediated Oxidative Stress and Regulated Cell Death Signaling in Cancer

2021 ◽  
pp. 1-16
Author(s):  
Chandramani Pathak ◽  
Foram U. Vaidya ◽  
Bhargav N. Waghela ◽  
Abu Sufiyan Chhipa ◽  
Budhi Sagar Tiwari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Regulated Cell Death ◽  
Glycation End Products ◽  
End Products ◽  
Cell Death Signaling

scholarly journals Extracellular superoxide released from mitochondria mediates mast cell death by advanced glycation end products

2008 ◽  
Vol 1783 (12) ◽  
pp. 2332-2343 ◽  
Author(s):  
Tetsuro Yoshimaru ◽  
Yoshihiro Suzuki ◽  
Toshio Inoue ◽  
Shigeru Nishida ◽  
Chisei Ra
Keyword(s):  
Cell Death ◽  
Mast Cell ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death:A non-clinical study

2020 ◽  
Author(s):  
Takanobu Takata ◽  
Akiko Sakasai-Sakai ◽  
Masayoshi Takeuchi
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Advanced Glycation End Products ◽  
C2c12 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Myoblast Cell ◽  
And Function

Abstract Background: Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although sarcopenia is associated with lifestyle-related diseases (LSRD), the mechanisms underlying cell death in myoblasts, which differentiate to myotubes, remain unclear. We previously designated glyceraldehyde (an intermediate of glucose/fructose metabolism)-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in LSRD, and hypothesized that TAGE contribute to cell death in myoblasts. Methods: C2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2H-tetrazole-3-ium (WST-8) and slot blot assays. Cells were pretreated with 8 mM aminoguanidine , an inhibitor of AGE production, for 2 h, followed by 0, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE levels were then assessed. Serum TAGE levels in STAM mice, in which there were four stages (no steatosis, simple steatosis, steatohepatitis, and fibrosis), were measured using a competitive enzyme-linked immunosorbent assay. Results were expressed as TAGE units (U) per milliliter of serum, with 1 U corresponding to 1.0 μg of glyceraldehyde-derived AGE-bovine serum albumin (BSA) (TAGE-BSA). The viability of cells treated with 20, 50, and 100 μg/mL non-glycated BSA and TAGE-BSA for 24 h was assessed using the WST-8 assay. Results: In C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% ( p =0.0021) and 5.0% ( p =0.0001) and intracellular TAGE levels increased to 6.0 and 15.9 μg/mg protein, respectively. Changes in cell viability and TAGE production were completely inhibited by 8 mM aminoguanidine. Serum TAGE levels at the steatohepatitis and fibrosis stages were 10.51 ±1.16 and 10.44±0.95 U/mL, respectively, and were higher than those at the no steatosis stage ( 7.27 ±0.18 U/mL). Cell death was not induced by 20 or 50 μg/mL TAGE-BSA. The viabilities of C2C12 cells treated with 100 μg/mL non-glycated BSA and TAGE-BSA were 105.0% ( p =0.2890) and 85.3% ( p =0.0217), respectively. Conclusion: Intracellular TAGE strongly induced cell death in C2C12 cells and may also induce myoblast cell death in LSRD model mice.

scholarly journals Apelin attenuated advanced glycation end products-induced cell death in mouse endothelial cell line bEnd.3.

2021 ◽  
Vol 94 (0) ◽  
pp. 1-P2-09
Author(s):  
Yasuhiro Yoshioka ◽  
Haruku Yamamoto ◽  
Shigenori Yoshizawa ◽  
Akiko Yamamuro ◽  
Yuki Ishimaru ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Cell Line ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Endothelial Cell Line ◽  
Glycation End Products ◽  
End Products

scholarly journals Protective Effects of the Soluble Receptor for Advanced Glycation End-Products on Pyroptosis during Myocardial Ischemia-Reperfusion

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yingming Liu ◽  
Xinying Guo ◽  
Jie Zhang ◽  
Xuejie Han ◽  
Hongxia Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Advanced Glycation End Products ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Soluble Receptor ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Myocardial Ischemia Reperfusion

Ischemia-reperfusion injury (IRI) is an inevitable process when reperfusion therapy undergoes in acute myocardial infarction patients, which will lead to cardiac cell death. Many factors have been found to protect the myocardium, one of which was the soluble receptor for advanced glycation end-products (sRAGE) that protected the myocardium from apoptosis and autophagy. However, pyroptosis is also an important form of cell death that occurs during ischemia-reperfusion (I/R), whose critical molecule, NLR family pyrin domain containing 3 (NLRP3), was ever reported to be inhibited by sRAGE; therefore, it is hypothesized that sRAGE may decrease the cardiac pyroptosis induced by I/R. The results showed that sRAGE protected cardiomyocytes from I/R-induced pyroptosis by decreasing the expression level of NLRP3, gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18). Meanwhile, the results from primary cultured cardiomyocytes showed that the NF-κB pathway mediated the effects of sRAGE on pyroptosis. Therefore, it is concluded that sRAGE protects the heart from pyroptosis through inhibiting the NF-κB pathway during myocardial ischemia-reperfusion.

scholarly journals Impact of intracellular toxic advanced glycation end-products (TAGE) on murine myoblast cell death: A non-clinical study

2020 ◽  
Author(s):  
Takanobu Takata ◽  
Akiko Sakasai-Sakai ◽  
Masayoshi Takeuchi
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Advanced Glycation End Products ◽  
C2c12 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Underlying Mechanisms ◽  
Myoblast Cell

Abstract Background: Sarcopenia is a progressive condition that is characterized by decreases in skeletal muscle mass and function. Although previous studies reported that sarcopenia is associated with non-alcoholic steatohepatitis (NASH), the underlying mechanisms remain unclear. We herein focused on glyceraldehyde, an intermediate of glucose/fructose metabolism. We previously designated glyceraldehyde-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) because of their cytotoxicity and involvement in lifestyle-related diseases, such as NASH. We hypothesized that TAGE is associated with sarcopenia. Methods: C2C12 cells, which are murine myoblasts, were treated with 0, 0.5, 1, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed using 5-[2,4,-Bis(sodioxysulfonyl)phenyl]-3-(2-methoxy-4-nitrophenyl)-2-(4-nitrophenyl)-2H-tetrazole-3-ium (WST-8) and slot blot assays. Cells were pretreated with 8 mM aminoguanidine , an inhibitor of AGE production, for 2 h followed by 0, 1.5, and 2 mM glyceraldehyde for 24 h. Cell viability and intracellular TAGE were then assessed. Serum TAGE levels in STAM mice, in which there were four stages (no steatosis, simple steatosis, steatohepatitis, and fibrosis), were measured using an enzyme-linked immunosorbent assay. Results were expressed as TAGE units (U) per milliliter of serum, with 1 U corresponding to 1.0 μg of glyceraldehyde-derived AGE-bovine serum albumin (BSA) (TAGE-BSA). The viability of cells treated with 20, 50, and 100 μg/mL non-glycated BSA and TAGE-BSA for 24 h was assessed using the WST-8 assay. Results: In C2C12 cells treated with 1.5 and 2 mM glyceraldehyde, cell viability decreased to 47.7% ( p =0.0021) and 5.0% ( p =0.0001) and intracellular TAGE levels increased to 6.0 and 15.9 μg/mg protein, respectively. Changes in cell viability and TAGE production were completely inhibited by 8 mM aminoguanidine. Serum TAGE levels at the steatohepatitis and fibrosis stages were 10.51 ±1.16 and 10.44±0.95 U/mL, respectively, and were higher than that at the no steatosis stage (7.27±0.18 U/mL). Cell death was not induced by 20 or 50 μg/mL TAGE-BSA. The viabilities of C2C12 cells treated with 100 μg/mL non-glycated BSA and TAGE-BSA were 105.0% ( p =0.2890) and 85.3% ( p =0.0217), respectively. Conclusion: Intracellular TAGE strongly induce myoblast cell death and may cause sarcopenia. Therefore, TAGE may play a crucial role in sarcopenia associated with NASH .

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