scholarly journals Coregulation of Neurite Outgrowth and Cell Survival by Amphoterin and S100 Proteins through Receptor for Advanced Glycation End Products (RAGE) Activation

2000 ◽  
Vol 275 (51) ◽  
pp. 40096-40105 ◽  
Author(s):  
Henri J. Huttunen ◽  
Juha Kuja-Panula ◽  
Guglielmo Sorci ◽  
Anna Lisa Agneletti ◽  
Rosario Donato ◽  
...  
Keyword(s):  
Cell Survival ◽  
Neurite Outgrowth ◽  
Advanced Glycation End Products ◽  
S100 Proteins ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals The Effect of Glyceraldehyde-Derived Advanced Glycation End Products on β-Tubulin-Inhibited Neurite Outgrowth in SH-SY5Y Human Neuroblastoma Cells

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2958
Author(s):  
Ryuto Nasu ◽  
Ayako Furukawa ◽  
Keita Suzuki ◽  
Masayoshi Takeuchi ◽  
Yoshiki Koriyama
Keyword(s):  
Neurite Outgrowth ◽  
Advanced Glycation End Products ◽  
Neurological Disorders ◽  
Neuroblastoma Cells ◽  
Advanced Glycation ◽  
Human Neuroblastoma ◽  
Increased Risk ◽  
Glycation End Products ◽  
End Products ◽  
Β Tubulin

Nutritional factors can affect the risk of developing neurological disorders and their rate of progression. In particular, abnormalities of carbohydrate metabolism in diabetes mellitus patients lead to an increased risk of neurological disorders such as Alzheimer’s disease (AD). In this study, we investigated the relationship between nervous system disorder and the pathogenesis of AD by exposing SH-SY5Y neuroblastoma cells to glyceraldehyde (GA). We previously reported that GA-derived toxic advanced glycation end products (toxic AGEs, TAGE) induce AD-like alterations including intracellular tau phosphorylation. However, the role of TAGE and their target molecules in the pathogenesis of AD remains unclear. In this study, we investigated the target protein for TAGE by performing two-dimensional immunoblot analysis with anti-TAGE antibody and mass spectrometry and identified β-tubulin as one of the targets. GA treatment induced TAGE-β-tubulin formation and abnormal aggregation of β-tubulin, and inhibited neurite outgrowth in SH-SY5Y cells. On the other hand, glucose-derived AGEs were also involved in developing AD. However, glucose did not make abnormal aggregation of β-tubulin and did not inhibit neurite outgrowth. Understanding the underlying mechanism of TAGE-β-tubulin formation by GA and its role in neurodegeneration may aid in the development of novel therapeutics and neuroprotection strategies.

scholarly journals Advanced glycation end products influence oral cancer cell survival via Bcl-xl and Nrf-2 regulation in vitro

2017 ◽  
Vol 13 (5) ◽  
pp. 3328-3334 ◽  
Author(s):  
Shun-Yao Ko ◽  
Hshin-An Ko ◽  
Tzong-Ming Shieh ◽  
Tzong-Cherng Chi ◽  
Hong-I Chen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cell Survival ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Oral Cancer Cell ◽  
Glycation End Products ◽  
End Products ◽  
Cancer Cell Survival

scholarly journals Modulation of Vagal Sensory Neurons via High Mobility Group Box-1 and Receptor for Advanced Glycation End Products: Implications for Respiratory Viral Infections

2021 ◽  
Vol 12 ◽  
Author(s):  
Stuart B. Mazzone ◽  
Seung-Kwon Yang ◽  
Jennifer A. Keller ◽  
Juste Simanauskaite ◽  
Jaisy Arikkatt ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Advanced Glycation End Products ◽  
High Mobility ◽  
High Mobility Group ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Deficient Mice

Vagal sensory neurons contribute to the symptoms and pathogenesis of inflammatory pulmonary diseases through processes that involve changes to their morphological and functional characteristics. The alarmin high mobility group box-1 (HMGB1) is an early mediator of pulmonary inflammation and can have actions on neurons in a range of inflammatory settings. We hypothesized that HMGB1 can regulate the growth and function of vagal sensory neurons and we set out to investigate this and the mechanisms involved. Culturing primary vagal sensory neurons from wildtype mice in the presence of HMGB1 significantly increased neurite outgrowth, while acute application of HMGB1 to isolated neurons under patch clamp electrophysiological investigation produced inward currents and enhanced action potential firing. Transcriptional analyses revealed the expression of the cognate HMGB1 receptors, Receptor for Advanced Glycation End products (RAGE) and Toll-like Receptor 4 (TLR4), in subsets of vagal sensory neurons. HMGB1-evoked growth and electrophysiological responses were significantly reduced in primary vagal sensory neurons harvested from RAGE deficient mice and completely absent in neurons from RAGE/TLR4 double deficient mice. Immunohistochemical analysis of vagal sensory neurons collected from mice after intranasal infection with murine pneumovirus or influenza A virus (IAV), or after intratracheal administration with the viral mimetic PolyI:C, revealed a significant increase in nuclear-to-cytoplasm translocation of HMGB1 compared to mock-inoculated mice. Neurons cultured from virus infected wildtype mice displayed a significant increase in neurite outgrowth, which was not observed for neurons from virus infected RAGE or RAGE/TLR4 deficient mice. These data suggest that HMGB1 can enhance vagal sensory neuron growth and excitability, acting primarily via sensory neuron RAGE. Activation of the HMGB1-RAGE axis in vagal sensory neurons could be an important mechanism leading to vagal hyperinnervation and hypersensitivity in chronic pulmonary disease.

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