Masahiro Watanabe
Shujitsu University
GeneInternal medicineEndocrinologyGlycationGene expressionThermogenesisMolecular biologyProinflammatory cytokineReceptorTumor necrosis factor alphaChemistryApoptosisInflammationRAGE (receptor)CytokineBrown adipose tissueCancer researchBiochemistryMedicineMicroarray analysis techniquesBiologyCell biology
24Publications
7H-index
207Citations
Publications 25
Newest
#1Yui Yamazaki (Kindai University)H-Index: 3
#2Hidenori Wake (Kindai University)
Last. Masahiro NishiboriH-Index: 51
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Abstract null null Toxic advanced glycation end products (toxic AGEs) derived from glycolaldehyde (AGE3) have been implicated in the development of diabetic vascular complications such as retinopathy characterised by excessive angiogenesis. Different receptor types, such as receptor for AGEs (RAGE), Toll like receptor-4 and scavenger receptors, are expressed in endothelial cells and contribute to AGE-elicited alteration of cell function. In the present study, we examined the involvement of AGE-r...
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#1Shuji Mori (Shujitsu University)H-Index: 17
#2Masahiro Watanabe (Shujitsu University)H-Index: 7
Last. Takao Toyomura (Shujitsu University)H-Index: 2
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#1Masahiro Watanabe (Shujitsu University)H-Index: 7
#2Takao Toyomura (Shujitsu University)H-Index: 2
Last. Shuji Mori (Shujitsu University)H-Index: 17
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Previously, we found that advanced glycation endproducts (AGEs) directly interact with tumor necrosis factor (TNF)-like weak inducer of apoptosis, a cytokine that controls inflammation, and that this interaction inhibited its action. This finding raised the novel possibility that AGEs alter the function of other cytokines through direct interaction. To investigate this possibility, we performed comprehensive screening for candidates that interacted with AGEs using protein array analysis. The arr...
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#1Masahiro Watanabe (Shujitsu University)H-Index: 7
#2Takao Toyomura (Shujitsu University)H-Index: 2
Last. Shuji Mori (Shujitsu University)H-Index: 17
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: Advanced glycation end products (AGEs) are considered to be related to the pathogenesis of some inflammatory diseases. AGEs were reported to stimulate the receptor for AGEs (RAGE), which causes inflammatory reactions. However, recently, toll-like receptors (TLRs), in addition to RAGE, have been reported to be related to AGE-mediated cellular responses, and it remains unclear which receptor is responsible for AGE recognition. To reveal the role of pattern-recognition receptors, including TLRs a...
9 CitationsSource
Advanced glycation end products (AGEs) are non-enzymatically formed from sugars or their metabolites with biomolecules. These molecules are formed in vivo, and the formation of AGEs on functional biomolecules was demonstrated to alter their properties. In addition, AGEs were reported to elicit inflammatory reactions by stimulating their endogenous receptors. However, the relationship between AGEs and these phenomena remains unclear. To understand the pathophysiological roles of AGEs, we investig...
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#1Shuji Mori (Shujitsu University)H-Index: 17
#2Masahiro Watanabe (Shujitsu University)H-Index: 7
Last. Takao Toyomura (Shujitsu University)H-Index: 2
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#1Tatsuya Tai (Kagawa University)
#2Kazunori Yamaguchi (Kagawa University)H-Index: 4
Last. Hitoshi Hochi (Kagawa University)
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#1Masahiro Watanabe (Shujitsu University)H-Index: 7
#2Takao Toyomura (Shujitsu University)H-Index: 2
Last. Shuji Mori (Shujitsu University)H-Index: 17
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: Previously, we found that endogenously produced pro-inflammatory molecules, advanced glycation end products (AGEs), interact with tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and attenuate its immunomodulatory function. In the present study, to elucidate the mechanism by which AGEs attenuate TWEAK function, we searched for regions responsible for TWEAK-AGE interaction using TWEAK deletion mutants. Pull-down assays with the TWEAK mutants and AGEs revealed that the C-terminal ha...
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#1Shuji Mori (Shujitsu University)H-Index: 17
#2Masahiro Watanabe (Shujitsu University)H-Index: 7
Last. Takao Toyomura (Shujitsu University)H-Index: 2
view all 8 authors...
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