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rage-receptor-for-age

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Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):595-P
Published: 01 July 2018
... and RAGE in human retinal pigment epithelial (RPE) cells. We used h1RPE7, human RPE cells, damaged by 20 µM hydroquinone (HQ)+300 µg/mL advanced glycation end-product (AGE) as an experimental AMD model. These cells were treated with atorvastatin (100 nM) or lovastatin (2 µM) for 24 hours. After...
Images
Signaling network of vascular hyperglycemic memory. Hyperglycemia via SIRT1...
Published: 17 May 2013
FIG. 1. Signaling network of vascular hyperglycemic memory. Hyperglycemia via SIRT1 downregulation leads to acetylation of p53, NF-κB subunit p65, and histone 3 bound to p66Shc promoter. Activation of p53 leads to increased p66Shc transcription. In addition, glucose-induced GCN5 downregulation causes H3 acetylation and subsequent p66Shc transcription through chromatin remodeling. p53 protein as well as epigenetic-driven upregulation of p66Shc leads to persistent mitochondrial ROS production, which maintains hyperglycemia-induced PKCβII overexpression and PKCβII-dependent eNOS inhibitory phosphorylation at Thr495 residue even after glucose normalization. p66Shc also downregulates MnSOD, further increasing ROS accumulation. These changes underlie endothelial dysfunction and apoptosis via reduced NO availability and activation of caspase 3 and PARP cleavage, respectively. SIRT1-p53-p66Shc networking via ROS production increases activity of the methyltransferase Set7/9, responsible for promoter monomethylation (H3K4 m) of NF-κB subunit p65 leading to its persistent transcription and subsequent upregulation of MCP-1 and VCAM-1 inflammatory genes. Ac, acetylation; p, phoshorylation; RAGE, receptor for AGEs. FIG. 1. Signaling network of vascular hyperglycemic memory. Hyperglycemia via SIRT1 downregulation leads to acetylation of p53, NF-κB subunit p65, and histone 3 bound to p66Shc promoter. Activation of p53 leads to increased p66Shc transcription. In addition, glucose-induced GCN5 downregulation causes H3 acetylation and subsequent p66Shc transcription through chromatin remodeling. p53 protein as well as epigenetic-driven upregulation of p66Shc leads to persistent mitochondrial ROS production, which maintains hyperglycemia-induced PKCβII overexpression and PKCβII-dependent eNOS inhibitory phosphorylation at Thr495 residue even after glucose normalization. p66Shc also downregulates MnSOD, further increasing ROS accumulation. These changes underlie endothelial dysfunction and apoptosis via reduced NO availability and activation of caspase 3 and PARP cleavage, respectively. SIRT1-p53-p66Shc networking via ROS production increases activity of the methyltransferase Set7/9, responsible for promoter monomethylation (H3K4 m) of NF-κB subunit p65 leading to its persistent transcription and subsequent upregulation of MCP-1 and VCAM-1 inflammatory genes. Ac, acetylation; p, phoshorylation; RAGE, receptor for AGEs. More
Images
Induction of autophagic flux by TFEB increases eNOS dimerization by lowerin...
Published: 18 February 2022
Figure 3 Induction of autophagic flux by TFEB increases eNOS dimerization by lowering ROS. (A) HUVECs were transfected with Ad-TFEB for 24 h and RNA sequencing was used to determine the transcriptome after TFEB overexpression. KEGG enrichment analysis results of the top enriched pathways are presented in a bubble plot. (B) Heat map data showing increased expression of autophagy and lysosomal biogenesis-associated genes by TFEB. HUVECs were transfected with Ad-GFP or Ad-TFEB for 24 h, then incubated with CQ (10 µmol/L) or BafA1 (10 nmol/L) under FBS-free conditions. (C) Representative images and statistical analysis of mtROS production measured by MitoSOX red staining in HUVECs treated with BafA1 (10 nmol/L, 3 h); n = 7–8. (D and E) Western blot was used to measure the protein levels of eNOS, TFEB, p62, and LC3 (12 h); n = 8. Results are reported as mean ± SD. Statistical analysis was performed using one-way ANOVA followed by Tukey test for (C and E). RAGE, receptor for AGEs. More
Journal Articles
Journal: Diabetes
Diabetes 1996;45(Supplement_3):S77–S80
Published: 01 July 1996
... means through which AGEs modulate cellular functions is through binding to specific cell surface acceptor molecules. The receptor for AGEs (RAGE) is such a receptor and is a newly identified member of the immunoglobulin superfamily expressed on endothelial cells (ECs), mononuclear phagocytes (MPs...
Journal Articles
Journal: Diabetes
Diabetes 2003;52(3):891–894
Published: 01 March 2003
..., particularly the receptor for AGEs (RAGE). Two functional polymorphisms in the promoter of the RAGE gene (−429 T/C and −374 T/A) and one in the AGE binding domain in exon 3 (G82S) were studied in 996 Finnish type 1 diabetic patients. In patients with poor metabolic control (HbA1c >9.5%), the AA...
Images
The link between diabetes and impaired RCT. Red arrows indicate pathways id...
Published: 18 November 2015
Figure 1 The link between diabetes and impaired RCT. Red arrows indicate pathways identified by Daffu et al. ( 12 ). In the setting of diabetes, RAGE ligands (i.e., AGE, S100A8/A9) become more abundant and there is enhanced RAGE expression on macrophages. A signaling event occurs downstream of RAG... More
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<span class="search-highlight">AGE</span>-induced activation of Smad3 was <span class="search-highlight">RAGE</span> mediated in MMECs. MMECs were cult...
Published: 03 August 2010
FIG. 5. AGE-induced activation of Smad3 was RAGE mediated in MMECs. MMECs were cultured in the presence of AGEs and BSA for 15–120 min or with different concentrations of AGEs for 30 min. Immunoprecipitation (IP) and Western blotting (WB) demonstrated the time course (A) and dose response (B) of Smad3 phosphorylation (p-Smad3) and total Smad3 levels in MMECs. C: MMECs were pretreated with control siRNA (CTL siRNA) or RAGE siRNA for 2 days and then cultured in the presence of BSA or AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated RAGE, p-Smad3, and total Smad3 in MMECs. D: MMECs were pretreated with goat anti-RAGE neutralizing antibody or goat IgG for 30 min and then cultured in the presence of AGEs. Upper panel: Immunoprecipitation/Western blotting demonstrated Smad3 phosphorylation and total Smad3 in MMECs. Lower panel: quantitation of arbitrary ratio of Smad3 phosphorylation/Smad3 in three independent experiments. a, vs. BSA-treated group, P < 0.05; b, vs. AGEs or AGEs plus goat IgG, P < 0.05. E: MMECs were pretreated with mouse anti–TGF-β1 neutralizing antibody or mouse IgG for 30 min and then cultured in the presence of AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated Smad3 Smad3 phosphorylation and total Smad3 in MMECs. F: MMECs were pretreated with control siRNA or TGF-β receptor 1 siRNA for 2 days and then cultured in the presence of AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated TGF-β receptor 1, GAPDH, p-Smad3, and total Smad3 in MMECs. FIG. 5. AGE-induced activation of Smad3 was RAGE mediated in MMECs. MMECs were cultured in the presence of AGEs and BSA for 15–120 min or with different concentrations of AGEs for 30 min. Immunoprecipitation (IP) and Western blotting (WB) demonstrated the time course (A) and dose response (B) of Smad3 phosphorylation (p-Smad3) and total Smad3 levels in MMECs. C: MMECs were pretreated with control siRNA (CTL siRNA) or RAGE siRNA for 2 days and then cultured in the presence of BSA or AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated RAGE, p-Smad3, and total Smad3 in MMECs. D: MMECs were pretreated with goat anti-RAGE neutralizing antibody or goat IgG for 30 min and then cultured in the presence of AGEs. Upper panel: Immunoprecipitation/Western blotting demonstrated Smad3 phosphorylation and total Smad3 in MMECs. Lower panel: quantitation of arbitrary ratio of Smad3 phosphorylation/Smad3 in three independent experiments. a, vs. BSA-treated group, P < 0.05; b, vs. AGEs or AGEs plus goat IgG, P < 0.05. E: MMECs were pretreated with mouse anti–TGF-β1 neutralizing antibody or mouse IgG for 30 min and then cultured in the presence of AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated Smad3 Smad3 phosphorylation and total Smad3 in MMECs. F: MMECs were pretreated with control siRNA or TGF-β receptor 1 siRNA for 2 days and then cultured in the presence of AGEs for 30 min. Immunoprecipitation/Western blotting demonstrated TGF-β receptor 1, GAPDH, p-Smad3, and total Smad3 in MMECs. More
Journal Articles
Journal: Diabetes
Diabetes 2004;53(10):2662–2668
Published: 01 October 2004
... to receptors for AGE (RAGEs) in vascular cells, thus inducing the expression of proinflammatory mediators. In animal models, interruption of the AGE-RAGE interaction reduces lesion size and plaque development. Therefore, limiting RAGE expression might be an intriguing concept to modulate vascular disease...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(10):2052–2058
Published: 01 October 1999
... binding to their endothelial receptor by intravenous bolus of soluble recombinant receptor to AGEs (rR-RAGE) (slope of extravasation versus time decreased by 19, 30, and 40%, for 0.5, 2.5, and 5.15 mg/kg rR-RAGE, respectively) or by a 6 mg/kg intravenous bolus of antibody against RAGE (slope decreased...
Journal Articles
Journal: Diabetes
Diabetes 2012;61(8):2105–2113
Published: 17 July 2012
... nephropathy that act through the receptor for AGEs (RAGE), as well as other mechanisms, to promote renal inflammation and glomerulosclerosis. The relative contribution of RAGE-dependent and RAGE-independent signaling pathways has not been previously studied in vivo. In this study, diabetic RAGE apoE...
Includes: Supplementary data
Images
Effect of <span class="search-highlight">RAGE</span> vaccine on urinary albumin and serum urea nitrogen and creat...
Published: 21 June 2021
Figure 6 Effect of RAGE vaccine on urinary albumin and serum urea nitrogen and creatinine levels in leptin receptor–deficient (db/db) mice. Male db/db mice were inoculated with the RAGE vaccine or KLH vehicle. A: Urine samples (n = 6/group) were obtained from mice just before immunization (prevaccination; age 10 weeks) and at 14 weeks after the final immunization (postvaccination; age 28 weeks), and the urine albumin-to-creatinine ratio was calculated. Sera (n = 5/group) were obtained from mice at 14 weeks after the final immunization, and serum urea nitrogen (B) and creatinine (C) were measured. Data are expressed as mean ± SEM, with differences between mean values evaluated for significance using the Student t test. *P < 0.05. Figure 6. Effect of RAGE vaccine on urinary albumin and serum urea nitrogen and creatinine levels in leptin receptor–deficient (db/db) mice. Male db/db mice were inoculated with the RAGE vaccine or KLH vehicle. A: Urine samples (n = 6/group) were obtained from mice just before immunization (prevaccination; age 10 weeks) and at 14 weeks after the final immunization (postvaccination; age 28 weeks), and the urine albumin-to-creatinine ratio was calculated. Sera (n = 5/group) were obtained from mice at 14 weeks after the final immunization, and serum urea nitrogen (B) and creatinine (C) were measured. Data are expressed as mean ± SEM, with differences between mean values evaluated for significance using the Student t test. *P < 0.05. More
Journal Articles
Journal: Diabetes
Diabetes 2004;53(1):166–172
Published: 01 January 2004
... pathway and through specific receptors for AGE (RAGEs). To explore a specific role for RAGE in renal changes in type 2 diabetes, we examined the renal effects of a neutralizing murine RAGE antibody in db/db mice, a model of obese type 2 diabetes. One group of db/db mice was treated for 2...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(6):1505–1511
Published: 01 June 2001
...Barry I. Hudson; Max H. Stickland; T. Simon Futers; Peter J. Grant Interactions between advanced glycation end products (AGEs) and the receptor for AGE (RAGE) are implicated in the vascular complications in diabetes. We have identified eight novel polymorphisms, of which the −1420 (GGT)n, −1393 G/T...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(6):1495–1504
Published: 01 June 2001
...Chen-Hsiung Yeh; Lydia Sturgis; Joe Haidacher; Xue-Nong Zhang; Sidney J. Sherwood; Robert J. Bjercke; Ondrej Juhasz; Michael T. Crow; Ronald G. Tilton; Larry Denner Advanced glycation end product (AGE) activation of the signal-transducing receptor for AGE (RAGE) has been linked to a proinflammatory...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(3):743–751
Published: 01 March 2004
...Jessica V. Valencia; Manisha Mone; Jin Zhang; Marla Weetall; Frank P. Buxton; Thomas E. Hughes Activation of the receptor for advanced glycation end products (RAGE) reportedly triggers a variety of proinflammatory responses. However, our previous work revealed that RAGE-binding AGEs free...
Journal Articles
Journal: Diabetes
Diabetes 2013;62(9):3241–3250
Published: 15 August 2013
...Yusuke Kaida; Kei Fukami; Takanori Matsui; Yuichiro Higashimoto; Yuri Nishino; Nana Obara; Yosuke Nakayama; Ryotaro Ando; Maki Toyonaga; Seiji Ueda; Masayoshi Takeuchi; Hiroyoshi Inoue; Seiya Okuda; Sho-ichi Yamagishi Advanced glycation end products (AGEs) and their receptor (RAGE) play a role...
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<span class="search-highlight">AGE</span> <span class="search-highlight">receptor</span> neutralization restores <span class="search-highlight">AGE</span>-mediated suppression of retinal an...
Published: 01 March 2005
FIG. 6. AGE receptor neutralization restores AGE-mediated suppression of retinal angiogenesis in vitro. A: Pretreatment of RMEC vascular tubes with an antibody to the AGE receptor galectin-3 restored AGE-BSA–mediated suppression of angiogenesis to the extent that there was no significant difference between BSA control–treated RMECs. B: Anti-RAGE antibody also reversed AGE-BSA–induced inhibition, although this pretreatment significantly enhanced the angiogenic response when compared with control subjects (P < 0.001). C: Galectin-3 neutralization also reversed diabetic serum–induced suppression of angiogenesis, restoring tube invasion to levels comparable to nondiabetic control subjects. FIG. 6. AGE receptor neutralization restores AGE-mediated suppression of retinal angiogenesis in vitro. A: Pretreatment of RMEC vascular tubes with an antibody to the AGE receptor galectin-3 restored AGE-BSA–mediated suppression of angiogenesis to the extent that there was no significant difference between BSA control–treated RMECs. B: Anti-RAGE antibody also reversed AGE-BSA–induced inhibition, although this pretreatment significantly enhanced the angiogenic response when compared with control subjects (P < 0.001). C: Galectin-3 neutralization also reversed diabetic serum–induced suppression of angiogenesis, restoring tube invasion to levels comparable to nondiabetic control subjects. More
Journal Articles
Journal: Diabetes
Diabetes 2007;56(3):647–655
Published: 01 March 2007
...James L. Figarola; Narkunaraja Shanmugam; Rama Natarajan; Samuel Rahbar Ligation of advanced glycation end products (AGEs) with their receptor (RAGE) plays an important role in the development of various diabetes complications, including atherosclerosis. Monocyte activation, adhesion, and migration...
Meeting Abstracts
Journal: Diabetes
Diabetes 2021;70(Supplement_1):1190-P
Published: 01 June 2021
... fibrosis. Type 2 diabetes (T2D) is an established risk factor for PDAC. The common mechanistic link might be the accumulation of advanced glycation end-products (AGEs) and the signaling through receptor for advanced glycation end-products (RAGE), the receptor for AGEs. Nevertheless, the role of RAGE...
Journal Articles
Journal: Diabetes
Diabetes 2021;70(9):2147–2158
Published: 21 June 2021
... and creatinine levels in leptin receptor–deficient (db/db) mice. Male db/db mice were inoculated with the RAGE vaccine or KLH vehicle. A: Urine samples (n = 6/group) were obtained from mice just before immunization (prevaccination; age 10 weeks) and at 14 weeks after the final immunization (postvaccination; age...