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Artykuły w czasopismach na temat „Receptors for advanced glycation end product (RAGE)”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 19 lutego 2022

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1

Mangalmurti, Nilam S., Jessica Friedman, Don L. Siegel, Janet Lee, and Steven M. Albelda. "Erythrocyte Advanced Glycation End-Products as Novel Mediators of Endothelial Dysfunction Following Transfusion." Blood 120, no. 21 (November 16, 2012): SCI—47—SCI—47. http://dx.doi.org/10.1182/blood.v120.21.sci-47.sci-47.

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Abstract Abstract SCI-47 Red cell transfusions are associated with the development of acute lung injury in critically ill patients, yet the mechanisms for this association remain unknown. We have previously shown that stored red blood cells (RBCs) express the advanced glycation end-product Nε-carboxymethyl lysine (Nε-CML) (1). Advanced glycation end-products (AGEs), a heterogeneous group of adducts formed during states of increased oxidative stress or hyperglycemia, are thought to exert their effects by binding to membrane receptors, including RAGE (the receptor for advanced glycation-end prod

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Wautier, Jean-Luc, and Marie-Paule Wautier. "Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders." International Journal of Molecular Sciences 21, no. 15 (July 27, 2020): 5315. http://dx.doi.org/10.3390/ijms21155315.

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In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cells (RBCs) in normal situations have little interaction with the endothelium. Abnormal adhesion of RBCs was first observed in sickle cell anemia involving vascular cell adhesion molecule (VCAM)-1, α4β1, Lu/BCAM, and intercellular adhesion molecule (ICAM)-4. More recently RBC adhesion was found to be

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Kuzan, Aleksandra, Emilia Królewicz, Karolina Nowakowska, Kamilla Stach, Krzysztof Kaliszewski, Paweł Domosławski, Łukasz Kotyra, Andrzej Gamian, and Irena Kustrzeba-Wójcicka. "Contribution of Glycation and Oxidative Stress to Thyroid Gland Pathology—A Pilot Study." Biomolecules 11, no. 4 (April 10, 2021): 557. http://dx.doi.org/10.3390/biom11040557.

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The patho-mechanism of changes in the thyroid gland, including carcinogenesis, is a complex process, which involves oxidative stress. The goal of our investigation was to verify the extent of stress in the thyroid gland related to glycation. The study samples were comprised of blood sera, thyroid, and adipose tissue sections probed from 37 patients diagnosed with thyroid cancers and goiter. Using immuno-enzymatic and fluorometric assays we analyzed the content of advanced glycation end-products (AGEs), pentosidine, receptors for advanced glycation end-products (RAGE), scavenger receptor class

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Buckley, Stephen T., and Carsten Ehrhardt. "The Receptor for Advanced Glycation End Products (RAGE) and the Lung." Journal of Biomedicine and Biotechnology 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/917108.

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The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface molecules. As a pattern-recognition receptor capable of binding a diverse range of ligands, it is typically expressed at low levels under normal physiological conditions in the majority of tissues. In contrast, the lung exhibits high basal level expression of RAGE localised primarily in alveolar type I (ATI) cells, suggesting a potentially important role for the receptor in maintaining lung homeostasis. Indeed, disruption of RAGE levels has been implicated in the pathogenesis o

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5

Jensen, Louise J. N., Allan Flyvbjerg, and Mette Bjerre. "Soluble Receptor for Advanced Glycation End Product: A Biomarker for Acute Coronary Syndrome." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/815942.

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The receptor of advanced glycation end products (RAGE) and its ligands are linked to the pathogenesis of coronary artery disease (CAD), and circulating soluble receptor of advanced glycation end products (sRAGE), reflecting the RAGE activity, is suggested as a potential biomarker. Elevated sRAGE levels are reported in relation to acute ischemia and this review focuses on the role of sRAGE as a biomarker for the acute coronary syndrome (ACS). The current studies demonstrated that sRAGE levels are elevated in relation to ACS, however during a very narrow time period, indicating that the time of

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Rouhiainen, Ari, Niko-Petteri Nykänen, Juha Kuja-Panula, Päivi Vanttola, Henri Huttunen, and Heikki Rauvala. "Inhibition of Homophilic Interactions and Ligand Binding of the Receptor for Advanced Glycation End Products by Heparin and Heparin-Related Carbohydrate Structures." Medicines 5, no. 3 (July 30, 2018): 79. http://dx.doi.org/10.3390/medicines5030079.

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Background: Heparin and heparin-related sulphated carbohydrates inhibit ligand binding of the receptor for advanced glycation end products (RAGE). Here, we have studied the ability of heparin to inhibit homophilic interactions of RAGE in living cells and studied how heparin related structures interfere with RAGE–ligand interactions. Methods: Homophilic interactions of RAGE were studied with bead aggregation and living cell protein-fragment complementation assays. Ligand binding was analyzed with microwell binding and chromatographic assays. Cell surface advanced glycation end product binding t

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Sotokawauchi, Ami, Takanori Matsui, Yuichiro Higashimoto, and Sho-ichi Yamagishi. "Fructose causes endothelial cell damage via activation of advanced glycation end products–receptor system." Diabetes and Vascular Disease Research 16, no. 6 (August 2, 2019): 556–61. http://dx.doi.org/10.1177/1479164119866390.

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Objective: Advanced glycation end products and their receptor – RAGE – in the adipose tissues contribute to metabolic derangements in fructose-fed rats. However, it remains unclear whether fructose could cause endothelial cell damage via the activation of AGE-RAGE. Methods: Intracellular advanced glycation end products were evaluated by dot blot analysis. Fructose-derived advanced glycation end products (Fruc-AGEs) were prepared by incubating bovine serum albumin with fructose for 8 weeks. Reactive oxygen species generation was measured using a fluorescent probe. Vascular cell adhesion molecul

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Zhou, Xiaoyan, Jie Weng, Jing Xu, Qiulin Xu, Weiju Wang, Weijin Zhang, Qiaobing Huang, and Xiaohua Guo. "Mdia1 is Crucial for Advanced Glycation End Product-Induced Endothelial Hyperpermeability." Cellular Physiology and Biochemistry 45, no. 4 (2018): 1717–30. http://dx.doi.org/10.1159/000487780.

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Background/Aims: Disruption of endothelial barrier integrity in response to advanced glycation end products (AEGs) stimulation contributes to vasculopathy associated with diabetes mellitus. Mammalian diaphanous-related formin (mDia1) has been reported to bind to the cytoplasmic domain of the receptor for advanced glycation end products (RAGE), which induces a series of cellular processes. This study directly evaluated the participation of mDia1 in AGE-induced hyperpermeability and revealed the precise intracellular signal transductions of this pathological process. Methods: Human umbilical vei

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Bohlender, Jürgen M., Sybille Franke, Günter Stein, and Gunter Wolf. "Advanced glycation end products and the kidney." American Journal of Physiology-Renal Physiology 289, no. 4 (October 2005): F645—F659. http://dx.doi.org/10.1152/ajprenal.00398.2004.

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Advanced glycation end products (AGEs) are a heterogeneous group of protein and lipids to which sugar residues are covalently bound. AGE formation is increased in situations with hyperglycemia (e.g., diabetes mellitus) and is also stimulated by oxidative stress, for example in uremia. It appears that activation of the renin-angiotensin system may contribute to AGE formation through various mechanisms. Although AGEs could nonspecifically bind to basement membranes and modify their properties, they also induce specific cellular responses including the release of profibrogenic and proinflammatory

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Eichhorst, Alexandra, Christoph Daniel, Rita Rzepka, Bettina Sehnert, Falk Nimmerjahn, Reinhard E. Voll, and Nina Chevalier. "Relevance of Receptor for Advanced Glycation end Products (RAGE) in Murine Antibody-Mediated Autoimmune Diseases." International Journal of Molecular Sciences 20, no. 13 (July 1, 2019): 3234. http://dx.doi.org/10.3390/ijms20133234.

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It is incompletely understood how self-antigens become targets of humoral immunity in antibody-mediated autoimmune diseases. In this context, alarmins are discussed as an important level of regulation. Alarmins are recognized by various receptors, such as receptor for advanced glycation end products (RAGE). As RAGE is upregulated under inflammatory conditions, strongly binds nucleic acids and mediates pro-inflammatory responses upon alarmin recognition, our aim was to examine its contribution to immune complex-mediated autoimmune diseases. This question was addressed employing RAGE−/− animals

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Miyazaki, Dai, Michiko Kandori-Inoue, Yumiko Shimizu, Fumie Ohtani, Ikuyo Chono, Yoshitsugu Inoue, and Satoru Yamagami. "Role Played by Receptors for Advanced Glycosylation End Products in Corneal Endothelial Cells after HSV-1 Infection." International Journal of Molecular Sciences 22, no. 11 (May 29, 2021): 5833. http://dx.doi.org/10.3390/ijms22115833.

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Senescence, sterile inflammation, and infection cause dysfunction of corneal endothelial cells, leading to visual morbidity that may require corneal transplantation. With increasing age, the extracellular matrix is modified by non-enzymatic glycation forming advanced glycation end products (AGEs). The modifications are primarily sensed by the receptors for the AGEs (RAGE) and are manifested as a type I interferon response. Interestingly, in our study, human corneal endothelial cells (HCEn) cells did not respond to the typical RAGE ligands, including the AGEs, high mobility group box 1 (HMGB1),

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Borriello, Iannuzzi, and Sirangelo. "Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin." Cells 8, no. 5 (April 26, 2019): 385. http://dx.doi.org/10.3390/cells8050385.

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Advanced glycation end products (AGEs) are the end products of the glycation reaction and have a great importance in clinical science for their association with oxidative stress and inflammation, which play a major role in most chronic diseases, such as cardiovascular disease, neurodegenerative diseases, and diabetes. Their pathogenic effects are generally induced by the interaction between AGEs and the receptor for advanced glycation end product (RAGE) on the cell surface, which triggers reactive oxygen species production, nuclear factor kB (NF-kB) activation, and inflammation. Pinocembrin, t

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Uspenskaya, Yuliya Aleksandrovna, Yuliya Konstantinovna Komleva, Elena Anatol'evna Pozhilenkova, Vladimir Valer'evic Salmin, Ol'ga Leonidovna Lopatina, Aleksandr Anatol'evich Fursov, Pavel Vyacheslavovich Lavrent'ev, Ol'ga Anatol'evna Belova, and Alla Borisovna Salmina. "Ligands of RAGE-Proteins: Role in Intercellular Communication and Pathogenesis of Inflammation." Annals of the Russian academy of medical sciences 70, no. 6 (December 8, 2015): 694–703. http://dx.doi.org/10.15690/vramn566.

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The review contains data on the diversity of endogenous ligands of RAGE receptors (receptor for advanced glycation end products) that play an important role in the signal transduction in (patho) physiological conditions. RAGE takes part in various physiological processes like cell growth and survival, apoptosis and regeneration. They serve as regulators of inflammatory reactions due to their ability to induce secretion of cytokines and chemokines. In addition, they facilitate elimination of apoptotic cells and mediate innate immune response. We discuss mechanisms of soluble RAGE production as

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14

Prasad, Chandan, Kathleen E. Davis, Victorine Imrhan, Shanil Juma, and Parakat Vijayagopal. "Advanced Glycation End Products and Risks for Chronic Diseases: Intervening Through Lifestyle Modification." American Journal of Lifestyle Medicine 13, no. 4 (May 15, 2017): 384–404. http://dx.doi.org/10.1177/1559827617708991.

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Advanced glycation end products (AGEs) are a family of compounds of diverse chemical nature that are the products of nonenzymatic reactions between reducing sugars and proteins, lipids, or nucleic acids. AGEs bind to one or more of their multiple receptors (RAGE) found on a variety of cell types and elicit an array of biologic responses. In this review, we have summarized the data on the nature of AGEs and issues associated with their measurements, their receptors, and changes in their expression under different physiologic and disease states. Last, we have used this information to prescribe l

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Tesarova, P., M. Kalousova, M. Jachymova, O. Mestek, L. Petruzelka, and T. Zima. "Receptor for advanced glycation end-products (RAGE) - soluble form (sRAGE) and gene polymorphisms in patients with breast cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 21113. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21113.

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21113 Background: Receptor for advanced glycation end products (RAGE) may be involved in the pathogenesis of the cancer progression and metastasis. Pathological effects mediated via RAGE are physiologically inhibited by soluble RAGE (sRAGE), so the higher sRAGE levels may confer the patients with cancer with better outcome.. Our aim was to study sRAGE and RAGE gene polymorphisms in patients with breast cancer. Methods: We studied sRAGE and RAGE polymorphisms in 120 patients with breast cancer (subdivided based on the clinical stage, histologic grading, expression of hormonal and C-erb B2 recep

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Bakunina, Natalya Sergeyevna, Ruslan Ivanovich Glushakov, Natalya Igorevna Tapilskaya, and Petr Dmitriyevich Shabanov. "Pharmacology of polyprenols as adaptogens reducing glycation processes." Reviews on Clinical Pharmacology and Drug Therapy 11, no. 4 (December 15, 2013): 44–53. http://dx.doi.org/10.17816/rcf11444-53.

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Nowadays a significant attention is currently given to the process of glycation which plays an important role in the pathogenesis of vascular complications of diabetes and different neurodegenerative diseases. As a result of inconvertible transformation of early glycation products, stable compounds with different structure are produced - advanced glycation end-products (AGE), which have special patterns leading to pathological development. There are specific receptors of AGE which include phagocyte receptor, RAGE-receptor for advanced glycation end products, and galectin-3. It is necessary to

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Serveaux-Dancer, Marine, Matthieu Jabaudon, Isabelle Creveaux, Corinne Belville, Raïko Blondonnet, Christelle Gross, Jean-Michel Constantin, Loïc Blanchon, and Vincent Sapin. "Pathological Implications of Receptor for Advanced Glycation End-Product (AGER) Gene Polymorphism." Disease Markers 2019 (February 4, 2019): 1–17. http://dx.doi.org/10.1155/2019/2067353.

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The receptor for advanced glycation end-products (RAGE) is a cell surface transmembrane multiligand receptor, encoded by the AGER gene. RAGE presents many transcripts, is expressed mainly in the lung, and involves multiple pathways (such as NFκB, Akt, p38, and MAP kinases) that initiate and perpetuate an unfavorable proinflammatory state. Due to these numerous functional activities, RAGE is implicated in multiple diseases. AGER is a highly polymorphic gene, with polymorphisms or SNP (single-nucleotide polymorphism) that could be responsible or co-responsible for disease development. This revie

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Chen, Lixian, Yun Cui, Bingyu Li, Jie Weng, Weiju Wang, Shuangshuang Zhang, Xuliang Huang, Xiaohua Guo, and Qiaobing Huang. "Advanced glycation end products induce immature angiogenesis in in vivo and ex vivo mouse models." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 3 (March 1, 2020): H519—H533. http://dx.doi.org/10.1152/ajpheart.00473.2019.

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Proliferative diabetic retinopathy (PDR) is a progressive disease predominantly involving pathological angiogenesis and is characterized by the development of immature, fragile, and easily hemorrhagic new vessels. Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) play important roles in the progression of diabetic retinopathy. Our previous studies demonstrated that AGEs promoted HUVEC angiogenesis by inducing moesin phosphorylation via RhoA/Rho-associated protein kinase (ROCK) pathway. The aim of this study was to further confirm AGE-induced angiogenesis in vivo and the i

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Sourris, Karly C., Brooke E. Harcourt, Sally A. Penfold, Felicia Y. T. Yap, Amy L. Morley, Philip E. Morgan, Michael J. Davies, Scott T. Baker, George Jerums, and Josephine M. Forbes. "Modulation of the Cellular Expression of Circulating Advanced Glycation End-Product Receptors in Type 2 Diabetic Nephropathy." Experimental Diabetes Research 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/974681.

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Background. Advanced glycation end-products (AGEs) and their receptors are prominent contributors to diabetic kidney disease.Methods. Flow cytometry was used to measure the predictive capacity for kidney impairment of the AGE receptors RAGE, AGE-R1, and AGE-R3 on peripheral blood mononuclear cells (PBMCs) in experimental models of type 2 diabetes (T2DM) fed varied AGE containing diets and in obese type 2 diabetic and control human subjects.Results. Diets high in AGE content fed to diabetic mice decreased cell surface RAGE on PBMCs and in type 2 diabetic patients with renal impairment (RI). All

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El-Far, Ali H., Grazyna Sroga, Soad K. Al Jaouni, and Shaker A. Mousa. "Role and Mechanisms of RAGE-Ligand Complexes and RAGE-Inhibitors in Cancer Progression." International Journal of Molecular Sciences 21, no. 10 (May 20, 2020): 3613. http://dx.doi.org/10.3390/ijms21103613.

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Interactions of the receptor for advanced glycation end product (RAGE) and its ligands in the context of their role in diabetes mellitus, inflammation, and carcinogenesis have been extensively investigated. This review focuses on the role of RAGE-ligands and anti-RAGE drugs capable of controlling cancer progression. Different studies have demonstrated interaction of RAGE with a diverse range of acidic (negatively charged) ligands such as advanced glycation end products (AGEs), high-mobility group box1 (HMGB1), and S100s, and their importance to cancer progression. Some RAGE-ligands displayed e

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Deng, Quanwen, Can Bu, Liqian Mo, Bin Lv, Shaolian Song, Xiaoyan Xiao, Guo Dan, and Xixiao Yang. "Huang Gan Formula Eliminates the Oxidative Stress Effects of Advanced Oxidation Protein Products on the Divergent Regulation of the Expression of AGEs Receptors via the JAK2/STAT3 Pathway." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/4520916.

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Chronic kidney disease (CKD) has a high prevalence and low cure rate and represents a significant health issue. Oxidative stress is common in CKD due to metabolic disorders, inflammation, and impaired renal function changing normal proteins into advanced oxidation protein products (AOPPs). Huang Gan formula (HGF) is a new type of traditional Chinese herbal medicine. Although we previously investigated the protective effects of HGF against oxidative stress, the mechanism of HGF in CKD is still not fully understood. In this study, we used western blotting, quantitative polymerase chain reaction,

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Khanam, Afreen, Saheem Ahmad, Arbab Husain, Shahnawaz Rehman, Alvina Farooqui, and Mohd Aslam Yusuf. "Glycation and Antioxidants: Hand in the Glove of Antiglycation and Natural Antioxidants." Current Protein & Peptide Science 21, no. 9 (December 11, 2020): 899–915. http://dx.doi.org/10.2174/1389203721666200210103304.

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The non-enzymatic interaction of sugar and protein resulting in the formation of advanced glycation end products responsible for cell signaling alterations ultimately leads to the human chronic disorders such as diabetes mellitus, cardiovascular diseases, cancer, etc. Studies suggest that AGEs upon interaction with receptors for advanced glycation end products (RAGE) result in the production of pro-inflammatory molecules and free radicals that exert altered gene expression effect. To date, many studies unveiled the potent role of synthetic and natural agents in inhibiting the glycation reactio

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Kumar Pasupulati, Anil, P. Swathi Chitra, and G. Bhanuprakash Reddy. "Advanced glycation end products mediated cellular and molecular events in the pathology of diabetic nephropathy." Biomolecular Concepts 7, no. 5-6 (December 1, 2016): 293–309. http://dx.doi.org/10.1515/bmc-2016-0021.

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AbstractDiabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients and a leading cause of end-stage renal disease (ESRD). Degenerative changes such as glomerular hypertrophy, hyperfiltration, widening of basement membranes, tubulointerstitial fibrosis, glomerulosclerosis and podocytopathy manifest in various degrees of proteinuria in DN. One of the key mechanisms implicated in the pathogenesis of DN is non-enzymatic glycation (NEG). NEG is the irreversible attachment of reducing sugars onto free amino groups of proteins by a series of events, which include the f

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Asadipooya, Kamyar, and Edilfavia Mae Uy. "Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature." Journal of the Endocrine Society 3, no. 10 (July 10, 2019): 1799–818. http://dx.doi.org/10.1210/js.2019-00160.

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AbstractDiabetes compromises bone cell metabolism and function, resulting in increased risk of fragility fracture. Advanced glycation end products (AGEs) interact with the receptor for AGEs (RAGE) and can make a meaningful contribution to bone cell metabolism and/or alter function. Searches in PubMed using the key words “advanced glycation end-product,” “RAGE,” “sRAGE,” “bone,” and “diabetes” were made to explain some of the clinical outcomes of diabetes in bone metabolism through the AGE–RAGE signaling pathway. All published clinical studies were included in tables. The AGE–RAGE signaling pat

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Sharma, Anil K., Var R. Sharma, Girish K. Gupta, Ghulam Md Ashraf, and Mohammad A. Kamal. "Advanced Glycation End Products (AGEs), Glutathione and Breast Cancer: Factors, Mechanism and Therapeutic Interventions." Current Drug Metabolism 20, no. 1 (March 11, 2019): 65–71. http://dx.doi.org/10.2174/1389200219666180912104342.

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Background: Advanced Glycation End products (AGEs) are basically the end result of glycation of proteins and/or lipids in the presence of sugars. Specific cases of hyperglycemia have been reported with increased propensity of generation of AGEs. Many chronic and deadly diseases such as diabetes, cancer and neurodegenerative disorders have been known to be caused as a result of generation of AGEs. The role of glutathione (GSH) metabolism and its intricate association with AGEs have also been well established in breast cancer prognosis and treatment. To understand the etiology, mechanism and pro

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Noguchi, Taketoshi, Toshiyuki Sado, Katsuhiko Naruse, Hiroshi Shigetomi, Akira Onogi, Shoji Haruta, Ryuji Kawaguchi, et al. "Evidence for Activation of Toll-Like Receptor and Receptor for Advanced Glycation End Products in Preterm Birth." Mediators of Inflammation 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/490406.

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Objective. Individuals with inflammation have a myriad of pregnancy aberrations including increasing their preterm birth risk. Toll-like receptors (TLRs) and receptor for advanced glycation end products (RAGE) and their ligands were all found to play a key role in inflammation. In the present study, we reviewed TLR and RAGE expression, their ligands, and signaling in preterm birth.Research Design and Methods. A systematic search was performed in the electronic databases PubMed and ScienceDirect up to July 2010, combining the keywords “preterm birth,” “TLR”, “RAGE”, “danger signal”, “alarmin”,

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Lee, Hee-Weon, Min Ji Gu, Yoonsook Kim, Jee-Young Lee, Seungju Lee, In-Wook Choi, and Sang Keun Ha. "Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE." Antioxidants 10, no. 9 (September 17, 2021): 1486. http://dx.doi.org/10.3390/antiox10091486.

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The glyoxal-lysine dimer (GOLD), which is a glyoxal (GO)-derived advanced glycation end product (AGE), is produced by the glycation reaction. In this study, we evaluated the effect of GOLD on the oxidative damage and inflammatory response in SV40 MES 13 mesangial cells. GOLD significantly increased the linkage with the V-type immunoglobulin domain of RAGE, a specific receptor of AGE. We found that GOLD treatment increased RAGE expression and reactive oxygen species (ROS) production in mesangial cells. GOLD remarkably regulated the protein and mRNA expression of nuclear factor erythroid 2-relat

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Yang, Fan, Zhe Wang, John H. Zhang, Jiping Tang, Xin Liu, Liang Tan, Qing-Yuan Huang, and Hua Feng. "Receptor for Advanced Glycation End-Product Antagonist Reduces Blood–Brain Barrier Damage After Intracerebral Hemorrhage." Stroke 46, no. 5 (May 2015): 1328–36. http://dx.doi.org/10.1161/strokeaha.114.008336.

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Background and Purpose— To determine whether the receptor for advanced glycation end-products (RAGE) plays a role in early brain injury from intracerebral hemorrhage (ICH), RAGE expression and activation after injury were examined in a rat model of ICH with or without administration of a RAGE-specific antagonist (FPS-ZM1). Methods— Autologous arterial blood was injected into the basal ganglia of rats to induce ICH. The motor function of the rats was examined, and water content was detected after euthanization. Blood–brain barrier permeability was determined by Evans blue staining and colloidal

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Grimm, Stefanie, Christiane Ott, Melanie Hörlacher, Daniela Weber, Annika Höhn, and Tilman Grune. "Advanced-glycation-end-product-induced formation of immunoproteasomes: involvement of RAGE and Jak2/STAT1." Biochemical Journal 448, no. 1 (October 18, 2012): 127–39. http://dx.doi.org/10.1042/bj20120298.

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AGEs (advanced glycation-end products) accumulate during aging and several pathologies such as Alzheimer's disease and diabetes. These protein products are known to inhibit proteolytic pathways. Moreover, AGEs are known to be involved in the activation of immune responses. In the present study we demonstrate that AGEs induce the expression of immunoproteasomal subunits. To elucidate a molecular basis underlying the observed effects we were able to demonstrate an activation of the Jak2 (Janus kinase 2)/STAT1 (signal transducer and activator of transcription 1) pathway. Inhibition of Jak2 by AG-

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Reynolds, Paul R., Stephen D. Kasteler, Manuel G. Cosio, Anne Sturrock, Tom Huecksteadt, and John R. Hoidal. "RAGE: developmental expression and positive feedback regulation by Egr-1 during cigarette smoke exposure in pulmonary epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 6 (June 2008): L1094—L1101. http://dx.doi.org/10.1152/ajplung.00318.2007.

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The receptor for advanced glycation end-products (RAGE) is a member of the immunoglobin superfamily of multiligand receptors. Following ligand binding, mechanisms associated with host defense, tissue remodeling, and inflammation are activated. RAGE is highly expressed in pulmonary epithelium transitioning from alveolar type (AT) II to ATI cells and is upregulated in the presence of ligand; however, the regulation and function of RAGE during development are less clear. Herein, immunohistochemistry demonstrated a temporal-spatial pattern of RAGE expression in pulmonary epithelial cells from embr

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Sirois, Cherilyn M., Tengchuan Jin, Allison L. Miller, Damien Bertheloot, Hirotaka Nakamura, Gabor L. Horvath, Abubakar Mian, et al. "RAGE is a nucleic acid receptor that promotes inflammatory responses to DNA." Journal of Experimental Medicine 210, no. 11 (September 30, 2013): 2447–63. http://dx.doi.org/10.1084/jem.20120201.

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Recognition of DNA and RNA molecules derived from pathogens or self-antigen is one way the mammalian immune system senses infection and tissue damage. Activation of immune signaling receptors by nucleic acids is controlled by limiting the access of DNA and RNA to intracellular receptors, but the mechanisms by which endosome-resident receptors encounter nucleic acids from the extracellular space are largely undefined. In this study, we show that the receptor for advanced glycation end-products (RAGE) promoted DNA uptake into endosomes and lowered the immune recognition threshold for the activat

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Prasad, Kailash, Abdullah Sarkar, Mohammad Zafar, Ahmed Shoker, Hamdi Moselhi, Maryann Tranquilli, Bulat Ziganshin, and John Elefteriades. "Advanced Glycation End Products and its Soluble Receptors in the Pathogenesis of Thoracic Aortic Aneurysm." AORTA 04, no. 01 (February 2016): 1–10. http://dx.doi.org/10.12945/j.aorta.2015.15.018.

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Background: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of thoracic aortic aneurysms (TAAs). Cytokines [Interleukin (IL)-Iβ, IL-2, IL-6, and TNF-α)] increase the expression of MMP-2 and -3. Advanced glycation end products (AGEs) interact with cell receptors to increase the release of cytokines. Circulating soluble receptors for AGEs (sRAGE) and endogenous secretory RAGE (esRAGE) compete with membrane bound RAGE for binding with AGEs and reduce the production of cytokines. It is hypothesized that low levels of serum sRAGE and esRAGE and high levels of AGEs, AGEs/sR

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Tancharoen, Salunya, Tassanee Tengrungsun, Theeralaksna Suddhasthira, Kiyoshi Kikuchi, Nuttavun Vechvongvan, Masayuki Tokuda, and Ikuro Maruyama. "Overexpression of Receptor for Advanced Glycation End Products and High-Mobility Group Box 1 in Human Dental Pulp Inflammation." Mediators of Inflammation 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/754069.

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High mobility group box 1 (HMGB1), a nonhistone DNA-binding protein, is released into the extracellular space and promotes inflammation. HMGB1 binds to related cell signaling transduction receptors, including receptor for advanced glycation end products (RAGE), which actively participate in vascular and inflammatory diseases. The aim of this study was to examine whether RAGE and HMGB1 are involved in the pathogenesis of pulpitis and investigate the effect of Prevotella intermedia (P. intermedia) lipopolysaccharide (LPS) on RAGE and HMGB1 expression in odontoblast-like cells (OLC-1). RAGE and H

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Nelson, Michael B., Adam C. Swensen, Duane R. Winden, Jared S. Bodine, Benjamin T. Bikman, and Paul R. Reynolds. "Cardiomyocyte mitochondrial respiration is reduced by receptor for advanced glycation end-product signaling in a ceramide-dependent manner." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 1 (July 1, 2015): H63—H69. http://dx.doi.org/10.1152/ajpheart.00043.2015.

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Cigarette smoke exposure is associated with an increased risk of cardiovascular complications. The role of advanced glycation end products (AGEs) is already well established in numerous comorbidities, including cardiomyopathy. Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function. Using an in vitro model, we treated H9C2 cardiomyocytes with the AGE carboxy-methyllysine before mitochondrial respiration assessment. We discovered that mitochondrial resp

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Chhipa, Abu Sufiyan, Swapnil P. Borse, Ruma Baksi, Sunali Lalotra, and Manish Nivsarkar. "Targeting receptors of advanced glycation end products (RAGE): Preventing diabetes induced cancer and diabetic complications." Pathology - Research and Practice 215, no. 11 (November 2019): 152643. http://dx.doi.org/10.1016/j.prp.2019.152643.

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Brinkley, Tina E., Richard D. Semba, Stephen B. Kritchevsky, and Denise K. Houston. "Dietary protein intake and circulating advanced glycation end product/receptor for advanced glycation end product concentrations in the Health, Aging, and Body Composition Study." American Journal of Clinical Nutrition 112, no. 6 (September 21, 2020): 1558–65. http://dx.doi.org/10.1093/ajcn/nqaa241.

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ABSTRACT Background Advanced glycation end products (AGEs) promote adverse health effects and may contribute to the multi-system functional decline observed in aging. Diet is a major source of AGEs, and foods high in protein may increase circulating AGE concentrations. However, epidemiological evidence that high-protein diets increase AGEs is lacking. Objectives We examined whether dietary protein intake was associated with serum concentrations of the major AGE carboxymethyl-lysine (CML) and the soluble receptor for AGEs (sRAGE) in 2439 participants from the Health, Aging, and Body Composition

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Bronowicka-Szydełko, Agnieszka, Łukasz Kotyra, Łukasz Lewandowski, Andrzej Gamian, and Irena Kustrzeba-Wójcicka. "Role of Advanced Glycation End-Products and Other Ligands for AGE Receptors in Thyroid Cancer Progression." Journal of Clinical Medicine 10, no. 18 (September 10, 2021): 4084. http://dx.doi.org/10.3390/jcm10184084.

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To date, thyroid cancers (TCs) remain a clinical challenge owing to their heterogeneous nature. The etiopathology of TCs is associated not only with genetic mutations or chromosomal rearrangements, but also non-genetic factors, such as oxidative-, nitrosative-, and carbonyl stress-related alterations in tumor environment. These factors, through leading to the activation of intracellular signaling pathways, induce tumor tissue proliferation. Interestingly, the incidence of TCs is often coexistent with various simultaneous mutations. Advanced glycation end-products (AGEs), their precursors and r

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Wu, Yidi, Wenwu Zhang, and Susan J. Gunst. "S100A4 is secreted by airway smooth muscle tissues and activates inflammatory signaling pathways via receptors for advanced glycation end products." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 1 (July 1, 2020): L185—L195. http://dx.doi.org/10.1152/ajplung.00347.2019.

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S100A4 is a low-molecular-mass (12 kDa) EF-hand Ca2+-binding S100 protein that is expressed in a broad range of normal tissue and cell types. S100A4 can be secreted from some cells to act in an autocrine or paracrine fashion on target cells and tissues. S100A4 has been reported in the extracellular fluids of subjects with several inflammatory diseases, including asthma. Airway smooth muscle plays a critical role in airway inflammation by synthesizing and secreting inflammatory cytokines. We hypothesized that S100A4 may play an immunomodulatory role in airway smooth muscle. Trachealis smooth mu

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Frank, Franziska, Veronika Bezold, Kaya Bork, Philip Rosenstock, Jonas Scheffler, and Rüdiger Horstkorte. "Advanced glycation endproducts and polysialylation affect the turnover of the neural cell adhesion molecule (NCAM) and the receptor for advanced glycation endproducts (RAGE)." Biological Chemistry 400, no. 2 (January 28, 2019): 219–26. http://dx.doi.org/10.1515/hsz-2018-0291.

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Abstract The balance between protein synthesis and degradation regulates the amount of expressed proteins. This protein turnover is usually quantified as the protein half-life time. Several studies suggest that protein degradation decreases with age and leads to increased deposits of damaged and non-functional proteins. Glycation is an age-dependent, non-enzymatic process leading to posttranslational modifications, so-called advanced glycation endproducts (AGE), which usually damage proteins and lead to protein aggregation. AGE are formed by the Maillard reaction, where carbonyls of carbohydra

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TANJI, NOZOMU, GLEN S. MARKOWITZ, CAIFENG FU, THOMAS KISLINGER, AKIHIKO TAGUCHI, MONIKA PISCHETSRIEDER, DAVID STERN, ANN MARIE SCHMIDT, and VIVETTE D. D'AGATI. "Expression of Advanced Glycation End Products and Their Cellular Receptor RAGE in Diabetic Nephropathy and Nondiabetic Renal Disease." Journal of the American Society of Nephrology 11, no. 9 (September 2000): 1656–66. http://dx.doi.org/10.1681/asn.v1191656.

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Abstract.Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major mechanisms,i.e., the alteration of extracellular matrix architecture through nonenzymatic glycation, with formation of protein crosslinks, and the modulation of cellular functions through interactions with specific cell surface receptors, the best characterized of which is the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may also be promoted by inflammatory processes and oxidative cellular injury. To characterize the distributions of AGE and RAGE in diabetic kidne

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Wilkinson, Kim, and Joseph El Khoury. "Microglial Scavenger Receptors and Their Roles in the Pathogenesis of Alzheimer's Disease." International Journal of Alzheimer's Disease 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/489456.

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Alzheimer’s disease (AD) is increasing in prevalence with the aging population. Deposition of amyloid-β(Aβ) in the brain of AD patients is a hallmark of the disease and is associated with increased microglial numbers and activation state. The interaction of microglia with Aβappears to play a dichotomous role in AD pathogenesis. On one hand, microglia can phagocytose and clear Aβ, but binding of microglia to Aβalso increases their ability to produce inflammatory cytokines, chemokines, and neurotoxic reactive oxygen species (ROS). Scavenger receptors, a group of evolutionally conserved proteins

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Li, Jie, Haiyan Shangguan, Xiaoqian Chen, Xiao Ye, Bin Zhong, Pen Chen, Yamei Wang, Bin Xin, Yan Bi, and Dalong Zhu. "Advanced glycation end product levels were correlated with inflammation and carotid atherosclerosis in type 2 diabetes patients." Open Life Sciences 15, no. 1 (June 11, 2020): 364–72. http://dx.doi.org/10.1515/biol-2020-0042.

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AbstractDiabetes mellitus with atherosclerosis (AS) adds to the social burden. This study aimed to investigate whether advanced glycation end product (AGE) levels were correlated with inflammation and carotid AS (CAS) in type 2 diabetes mellitus (T2DM) patients. A total of 50 elderly T2DM patients and 50 age-matched senior healthy subjects were recruited in this study. T2DM patients were classified into two groups based on the intima–media thickness (IMT) of the carotid artery from color Doppler ultrasonography. Patients with IMT > 1 mm were classified into the T2DM + CAS group (n = 28), an

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Cheng, Cailan L., Ying Tang, Zhenda Zheng, Xun Liu, Zengchun C. Ye, Cheng Wang, and Tanqi Q. Lou. "Advanced glycation end-products activate the renin-angiotensin system through the RAGE/PI3-K signaling pathway in podocytes." Clinical & Investigative Medicine 35, no. 5 (October 6, 2012): 282. http://dx.doi.org/10.25011/cim.v35i5.18701.

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Purpose: The purpose of this study was to investigate the effects of advanced glycation end-products (AGEs) on the components of the renin-angiotensin system (RAS) in podocytes and to understand the mechanism of these effects. Methods: Immortalized mouse podocytes were exposed to various concentrations of AGEs for different time intervals. The expression levels of angiotensinogen (AGT), angiotensin II type 1 and 2 receptors (AT1R and AT2R) and renin were examined by real-time PCR and western blot; the receptor for AGEs (RAGE) and both Akt and phosphorylated Akt were examined by western blot; l

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Ma, Ke, Yiming Xu, Chenchen Wang, Nan Li, Kexue Li, Yan Zhang, Xiaoyu Li, et al. "A cross talk between class a scavenger receptor and receptor for advanced glycation end-products contributes to diabetic retinopathy." American Journal of Physiology-Endocrinology and Metabolism 307, no. 12 (December 15, 2014): E1153—E1165. http://dx.doi.org/10.1152/ajpendo.00378.2014.

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In response to hyperglycemia in patients with diabetes, many signaling pathways contribute to the pathogenesis of diabetic complications, including diabetic retinopathy (DR). Excessive production of inflammatory mediators plays an important role in this process. Amadori-glycated albumin, one of the major forms of advanced glycated end-products, has been implicated in DR by inducing inflammatory responses in microglia/macrophages. Our goal was to delineate the potential cross talk between class A scavenger receptor (SR-A) and the receptor for advanced glycated end-product (RAGE) in the context

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Dinarvand, Peyman, Seyed Mahdi Hassanian, Shabir H. Qureshi, Chandrashekhara Manithody, Joel C. Eissenberg, Likui Yang, and Alireza R. Rezaie. "Polyphosphate amplifies proinflammatory responses of nuclear proteins through interaction with receptor for advanced glycation end products and P2Y1 purinergic receptor." Blood 123, no. 6 (February 6, 2014): 935–45. http://dx.doi.org/10.1182/blood-2013-09-529602.

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Key Points Extracellular nuclear proteins H4 and HMGB1 are highly proinflammatory cytokines. Inorganic polyP dramatically amplifies proinflammatory responses of H4 and HMGB1 through the RAGE and P2Y1 receptors.

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Buchs, A. E., A. Kornberg, M. Zahavi, D. Aharoni, C. Zarfati, and M. J. Rapoport. "Increased Expression of Tissue Factor and Receptor for Advanced Glycation End Products in Peripheral Blood Mononuclear Cells of Patients With Type 2 Diabetes Mellitus with Vascular Complications." Experimental Diabesity Research 5, no. 2 (2004): 163–69. http://dx.doi.org/10.1080/15438600490424325.

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The aim of the study was to determine the correlation between the expression of tissue factor (TF) and the receptor for advanced glycation end products (RAGEs) and vascular complications in patients with longstanding uncontrolled type 2 diabetes (T2D). TF and RAGE mRNAs as well as TF antigen and activity were investigated in 21 T2D patients with and without vascular complications. mRNA expression was assessed by reverse transcriptase–polymerase chain reaction (RT-PCR) in nonstimulated and advanced glycation end product (AGE) albumin–stimulated peripheral blood mononuclear cells (PBMCs). TF ant

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Ohira, Hideo, Atsuki Tsuruya, Daiki Oikawa, Wao Nakagawa, Rie Mamoto, Masahira Hattori, Toshiyuki Waki, Seiji Takahashi, Yoshio Fujioka, and Toru Nakayama. "Alteration of oxidative-stress and related marker levels in mouse colonic tissues and fecal microbiota structures with chronic ethanol administration: Implications for the pathogenesis of ethanol-related colorectal cancer." PLOS ONE 16, no. 2 (February 12, 2021): e0246580. http://dx.doi.org/10.1371/journal.pone.0246580.

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Chronic ethanol consumption is a risk factor for colorectal cancer, and ethanol-induced reactive oxygen species have been suggested to play important roles in the pathogenesis of ethanol-related colorectal cancer (ER-CRC). In this study, the effects of 10-week chronic administration of ethanol on the colonic levels of oxidative stress and advance glycation end product (AGE) levels, as well as fecal microbiota structures, were examined in a mouse model. Chronic oral administration of ethanol in mice (1.0 mL of 1.5% or 5.0% ethanol (v/v) per day per mouse, up to 10 weeks) resulted in the elevati

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Park, Jong Sung, Fabia Gamboni-Robertson, Qianbin He, Daiva Svetkauskaite, Jae-Yeol Kim, Derek Strassheim, Jang-Won Sohn, et al. "High mobility group box 1 protein interacts with multiple Toll-like receptors." American Journal of Physiology-Cell Physiology 290, no. 3 (March 2006): C917—C924. http://dx.doi.org/10.1152/ajpcell.00401.2005.

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High mobility group box 1 (HMGB1), originally described as a DNA-binding protein, can also be released extracellularly and functions as a late mediator of inflammatory responses. Although recent reports have indicated that the receptor for advanced glycation end products (RAGE) as well as Toll-like receptor (TLR)2 and TLR4 are involved in cellular activation by HMGB1, there has been little evidence of direct association between HMGB1 and these receptors. To examine this issue, we used fluorescence resonance energy transfer (FRET) and immunoprecipitation to directly investigate cell surface int

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Yuan, Gang, Guangyan Si, Qingchun Hou, Zhaonan Li, Kaiqiang Xu, Yuping Wang, Weiming Wang, et al. "Advanced Glycation End Products Induce Proliferation and Migration of Human Aortic Smooth Muscle Cells through PI3K/AKT Pathway." BioMed Research International 2020 (July 14, 2020): 1–11. http://dx.doi.org/10.1155/2020/8607418.

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Advanced glycation end products (AGEs) have been widely regarded as an important inducing factor in the pathogenesis of diabetic arteriosclerosis, and the proliferation and migration of vascular smooth muscle cells (VSMCs) are also involved in this process. However, it is not clear whether AGEs promote atherosclerosis by inducing the proliferation and migration of VSMCs. To figure out this question, this study investigated the effects of AGEs on the proliferation and migration of human aorta vascular smooth muscle cells (HASMCs) and the underlying mechanisms. This study evaluated the effects o

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Olejarz, Wioletta, Dominika Łacheta, Alicja Głuszko, Ewa Migacz, Wojciech Kukwa, Mirosław J. Szczepański, Piotr Tomaszewski, and Grażyna Nowicka. "RAGE and TLRs as Key Targets for Antiatherosclerotic Therapy." BioMed Research International 2018 (August 26, 2018): 1–10. http://dx.doi.org/10.1155/2018/7675286.

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Receptor for advanced glycation end-products (RAGE) and toll-like receptors (TLRs) are the key factors indicating a danger to the organism. They recognize the microbial origin pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). The primary response induced by PAMPs or DAMPs is inflammation. Excessive stimulation of the innate immune system occurs in arterial wall with the participation of effector cells. Persistent adaptive responses can also cause tissue damage and disease. However, inflammation mediated by the molecules innate responses is an impor

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