Relevant bibliographies by topics / Receptors for advanced glycation end product (RAGE)

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Receptors for advanced glycation end product (RAGE)'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Receptors for advanced glycation end product (RAGE)"

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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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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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Dissertations / Theses on the topic "Receptors for advanced glycation end product (RAGE)"

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Nelson, Michael Bruce. "The Role of Receptors for Advanced Glycation End-Products (RAGE) and Ceramide in Cardiovascular Disease." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/4423.

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Type 2 diabetes and cigarette smoke exposure are 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 carboxy-methyl lysine-BSA, followed by mitochondrial respiration assessment. We found that
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Jyoti, Faidat. "Development of New Antibody Based Theranostic Agents Targeting the Receptor for Advanced Glycation End-Product (Rage)." Diss., North Dakota State University, 2013. https://hdl.handle.net/10365/26866.

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The Receptor for Advanced Glycation End products (RAGE) interacts with several classes of structurally unrelated ligands. The activation of RAGE by its ligands results in the cellular activation of several kinases and transcription factors including mitogen activated protein kinases (MAPKs) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) resulting in sustained inflammation, which is involved in pathologies such as diabetes, cancer, Alzheimer's disease, multiple sclerosis and other diseases associated with chronic inflammation. Current mouse models of human disea
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Wood, Tyler Thomas. "Targeting of Receptors for Advanced Glycation End-Products (RAGE) Diminishes Acute Secondhand Smoke-Induced Inflammation in Mice." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4220.

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The receptor for advanced glycation end-products (RAGE) has increasingly been demonstrated to be an important modulator of inflammation in cases of pulmonary disease. Published reports involving tobacco smoke exposure have demonstrated increased expression of RAGE, its participation in pro-inflammatory signaling and its role in irreversible pulmonary remodeling. The current research evaluated for the first time the in vivo effects of short-term tobacco smoke exposure in RAGE null and control mice compared to identical animals exposed to room air only. Quantitative real time PCR, immunoblotting
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Alexander, Kristen Lena. "Differential Receptors for Advanced Glycation End-Products (RAGE) Expression in Preeclampsia, Intrauterine Growth Restriction and Gestational Diabetes." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/5463.

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Preeclampsia (PE), intrauterine growth restriction (IUGR) and gestational diabetes (GDM) increase the risk of maternal and fetal morbidity and mortality. The roles of Advanced Glycation End-products (AGEs) are already well documented concerning inflammation, hypoxia and oxidative stress. AGEs bind to its receptor, Receptor for Advanced Glycation End-products (RAGE), and activate an inflammatory pathway. This pathway alters the efficacy of invasive trophoblast cells and in the placenta and can result in placental dysfunction. We hypothesized that the placental dysfunction found in PE, IUGR, and
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Winden, Duane Ray. "Characterization of Secondhand Smoke (SHS) and Materno-Fetal Interactions in Receptors for Advanced Glycation End-Products (RAGE)-Targeted Mice." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4072.

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Receptors for advanced glycation end-products (RAGE) are pattern recognition receptors of the immunoglobulin superfamily highly expressed in the lung. Likely functions include the modulation of pulmonary inflammation during disease. However, the contributions of RAGE in the developing lung in cases where secondhand smoke (SHS) exposure occurs are unknown. In order to test the hypothesis that RAGE misexpression adversely affects lung morphogenesis, we exposed gestating dams to a controlled dose of SHS during the last four critical days of in utero lung morphogenesis. We discovered that both mat
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Robinson, Adam Benjamin. "The Pro-Inflammatory Contributions of Receptors for Advanced Glycation End-Products (RAGE) in Alveolar Macrophages Following Cigarette Smoke Exposure." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3253.

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Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors of the immunoglobin family expressed by epithelium and macrophages. RAGE expression increases following ligand binding and when diverse cells are exposed to a variety of insults including cigarette smoke extract (CSE). The current research sought to characterize the pro-inflammatory contributions of RAGE expressed by alveolar macrophages (AMs) following CSE exposure. Acute exposure of mice to CSE via nasal instillation revealed diminished bronchoalveolar lavage (BAL) cellularity and fewer AMs in RAGE n
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Chen, Suzi Su-Hsin, and suzi chen@med monash edu au. "Cyclooxygenase Expression in Human Diabetes." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080206.121439.

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Cyclooxygenase (COX) is the rate limiting enzyme that catalyses the production of prostanoids, which are crucial to vascular homeostasis. Evidence suggests that endothelial dysfunction and inflammation play a role in vascular complications in aging and diabetes. Previous animal studies by our laboratory at RMIT University reported enhanced COX expression with aging in rat aortas, platelets and monocytes. Potentially, alteration in COX expression may result in an imbalanced prostanoid production favoring the synthesis of vasoconstrictors and hence increase the risk of cardiovascular events in t
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Stogsdill, Jeffrey Alan. "Characterization of Altered Epithelial Cell Turnover and Differentiation in Embryonic Murine Lungs That Over-Express Receptors for Advanced Glycation End-Products (RAGE)." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3217.

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Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors highly expressed in the lung that modulate pulmonary inflammation during disease. However, the contributions of RAGE signaling are unknown during pulmonary organogenesis. In order to test the hypothesis that RAGE misexpression adversely affects lung morphogenesis, conditional transgenic mice were generated that over-express RAGE in alveolar type II cells of the lung. When RAGE is over-expressed throughout embryogenesis, severe lung hypoplasia ensues, culminating in perinatal lethality. Flow cytometry a
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Sirois, Cherilyn M. "Nucleic Acid Sensing by the Immune System: Roles For the Receptor For Advanced Glycation End Products (RAGE) and Intracellular Receptor Proteins: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/551.

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As humans, we inhabit an environment shared with many microorganisms, some of which are harmless or beneficial, and others which represent a threat to our health. A complex network of organs, cells and their protein products form our bodies’ immune system, tasked with detecting these potentially harmful agents and eliminating them. This same system also serves to detect changes in the healthy balance of normal functions in the body, and for repairing tissue damage caused by injury. Immune recognition of nucleic acids, DNA and RNA, is one way that the body detects invading pathogens and initiat
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Ren, Yimin. "Consequences of the interaction of amyloid beta with amyloid binding alcohol dehydrogenase and the receptor for advanced glycation end products." Thesis, St Andrews, 2008. http://hdl.handle.net/10023/503.

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Books on the topic "Receptors for advanced glycation end product (RAGE)"

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Kamal, Tarek. Significance of Advanced Glycation End-Products (AGE) and the Receptor for AGE (RAGE) in Diabetic Nephropathy. INTECH Open Access Publisher, 2012.

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Book chapters on the topic "Receptors for advanced glycation end product (RAGE)"

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Koyama, Hidenori, and Yoshiki Nishizawa. "Cardiovascular Complications in Renal Failure: Implications of Advanced Glycation End Products and Their Receptor RAGE." In Studies on Renal Disorders, 257–92. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-857-7_13.

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Khan, Rujman, Xin Yee Ooi, Matthew Parvus, Laura Valdez, and Andrew Tsin. "Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications." In The Eye and Foot in Diabetes. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89408.

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Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
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Kamal, Tarek, Yasuhiko Yamamoto, and Hiroshi Yamamoto. "Significance of Advanced Glycation End-Products (AGE) and the Receptor for AGE (RAGE) in Diabetic Nephropathy." In Diabetic Nephropathy. InTech, 2012. http://dx.doi.org/10.5772/34643.

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Fernando, Dinali H., Josephine M. Forbes, Peter W. Angus, and Chandana B. Herath. "The Receptor for Advanced Glycation End Products (RAGE): A Potential Target for Therapeutic Intervention in the Progression of Non-Alcoholic Fatty Liver Disease (NAFLD)." In Prime Archives in Molecular Biology. Vide Leaf, Hyderabad, 2020. http://dx.doi.org/10.37247/pamb.1.2020.25.

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Conference papers on the topic "Receptors for advanced glycation end product (RAGE)"

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Zhang, W., Y. Wu, and S. J. Gunst. "S100A4 Regulates Airway Smooth Muscle (ASM) Inflammation by Acting on Receptors for Advanced Glycation End Products (RAGE)." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2848.

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Wolf, Lisa, Julia Niederstraßer, Herr Christian, and Bals Robert. "Receptor for advanced glycation end products (RAGE) is involved in cigarette smoke induced inflammation and emphysema." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5048.

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Thompson, Ben, Alan Stitt, Cecilia O'Kane, and Danny McAuley. "Receptor For Advanced Glycation End Products (RAGE) Ligands Induce Pulmonary Endothelial And Epithelial Cell NF-?B Activation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5774.

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D'Souza, VK, CR Bassford, D. Park, F. Gao, DR Thickett, and GD Perkins. "The Receptor for Advanced Glycation End Products (RAGE) Is a Marker of Alveolar Epithelial Damage in ARDS." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3559.

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AI, Cabrera-García, M. Protschka, G. Alber, S. Kather, F. Dengler, U. Müller, JM Steiner, and RM Heilmann. "Dysregulation of gastrointestinal RAGE (receptor for advanced glycation end products) expression in dogs with inflammatory bowel disease." In 29. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 2: Poster. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1723879.

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Taniguchi, Akihiko, Nobuaki Miyahara, Arihiko Kanehiro, Koichi Waseda, Etsuko Kurimoto, Yasushi Tanimoto, Mikio Kataoka, et al. "Contrasting Roles For The Receptor For Advanced Glycation End-Products (RAGE) In Allergic Airway Inflammation Versus Airway Hyperresponsiveness." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4288.

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SHARMA, ASHISH K., Damien LaPar, Lucas Fernandez, and Victor Laubach. "Receptor For Advanced Glycation End Products (RAGE) And High Mobility Group Box 1 (HMGB1) Mediate Pulmonary Ischemia-Reperfusion Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5292.

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Bjerregaard, Asger, Celeste Porsbjerg, Lucy Barrett, Ingrid Laing, Siew-Kim Khoo, Markus Fally, Peter Le Souëf, Vibeke Backer, Philip Thompson, and Svetlana Baltic. "Signalling through the receptor for advanced glycation end products (RAGE) is increased in acute asthma and correlates with symptom severity." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa904.

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Retnaningtyas, Ekowati, Budi Susatia, Olly Indrajani, Verina Setyabudhi, and Hendry Santoso. "Hydrogen-rich water supplementation declines advanced glycation-end products (AGE) and receptor for AGE (RAGE) in streptozotocin-induced diabetic rats." In INTERNATIONAL CONFERENCE ON LIFE SCIENCES AND TECHNOLOGY (ICoLiST 2020). AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0052797.

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Reynolds, PR, RE Schmitt, SD Kasteler та JR Hoidal. "The Receptor for Advanced Glycation End Products (RAGE) Activates Ras and NFκ-β in Pulmonary Epithelial Cells Exposed to Cigarette Smoke." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4185.

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Reports on the topic "Receptors for advanced glycation end product (RAGE)"

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Ganju, Ramesh K. Receptor for Advanced Glycation End Products (RAGE) as a Novel Target for Inhibiting Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada592353.

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