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Noninvasive Sensing of Serum sRAGE and Glycated Hemoglobin by Skin UV-Induced Fluorescence
Published in Andrey V. Dunaev, Valery V. Tuchin, Biomedical Photonics for Diabetes Research, 2023
Vladimir V. Salmin, Tatyana E. Taranushenko, Natalya G. Kiseleva, Alla B. Salmina
Assessment of the level of RAGE expression in tissues may have some methodological difficulties (i.e., the need to obtain a histological sample and to perform immunohistochemistry, western blotting, or molecular genetic studies), while in the peripheral blood, sRAGE levels can be determined with the enzyme-linked immunoassay. A significant number of studies are currently focused on determining the diagnostic potential of data on actual sRAGE levels and their correlations with the expression of RAGE in tissues in normal and pathological conditions [42–44]. However, despite the well-established methods for the noninvasive assessment of collagen glycation products in the skin, there is a lack of noninvasive methods for the evaluation of sRAGE levels in the blood.
Neurodegeneration in Diabetes Mellitus
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Narsingh Verma, Smriti Rastogi
Vascular inflammation can also be mediated by the receptor for advanced glycation end products (RAGE). RAGE is expressed in neuronal cells, microglia astrocytes, and brain endothelial cells; its levels are increased in both Alzheimer’s and type 2 diabetes.28, 29 Increased RAGE levels have been proposed as a possible mechanism for vascular dysfunction in both Alzheimer’s and type 2 diabetes.30 The interactions between disturbed cerebral glucose metabolism, oxidative stress, and the accumulation of AGEs are important in the vicious cycle that contributes to the progression of Alzheimer’s disease.31 RAGE is an avenue for receptor-mediated transport of Aβ across the blood–brain barrier from the periphery to the brain,32 inducing cerebrovascular dysfunction, resulting in neurovascular stress, production of TNF-α and IL-6, and contributing to synaptoxicity and neurodegeneration.30
Chronic Fatigue Syndrome: Limbic Encephalopathy in a Dysregulated Neuroimmune Network
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
The irritability that CFS patients have is usually intermittent. Some patients relate it to frustration with the illness, and others cannot understand it. “Rage attacks” with violent lashing out are not infrequent. Certain medications for treatment of rage attacks (lithium, propanolol) are not effective, but others (buspirone, fluoxetine) may be. As with other CFS symptoms, if the entire syndrome improves, so does the irritability.
Pulmonary delivery of a recombinant RAGE antagonist peptide derived from high-mobility group box-1 in a bleomycin-induced pulmonary fibrosis animal model
Published in Journal of Drug Targeting, 2022
Chunxian Piao, Chuanyu Zhuang, Min Kyung Ko, Do Won Hwang, Minhyung Lee
Although some IPF treatments have improved patient outcomes, additional therapies based upon newly identified molecular factors underlying the pathogenesis of IPF should be developed. One of the important factors in progression of IPF is receptor for advanced glycation end products (RAGE) [19]. It was previously reported that knocking out the RAGE signal protected the lungs from IPF [20,21], suggesting RAGE inhibition as a target of IPF treatment. RAGE is a pattern recognition receptor for pro-inflammatory reactions [22,23] and is involved in various cellular activities such as proliferation, migration, inflammation and apoptosis [24]. The ligands for RAGE include high mobility group box-1 (HMGB-1), advanced glycation end products (AGEs), S100 protein and β-amyloid [23]. On binding with ligands, RAGE can activate the mitogen-activated protein kinase (MAPK) signal pathway, resulting in activation of nuclear factor-κB (NF-κB) [25,26]. Activation of the RAGE signalling pathway induces the expression of various genes, including those for pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) [27]. Therefore, RAGE signalling induces inflammatory reactions in lung diseases such as IPF and acute lung injury (ALI). In addition, activation of the RAGE signalling pathway induces RAGE gene expression, suggesting positive feedback regulation of RAGE [28].
Association of RAGE rs1800624 and rs1800625 gene polymorphisms with predisposition to optic neuritis and optic neuritis together with multiple sclerosis
Published in Ophthalmic Genetics, 2021
Gabriele Kolonaite, Alvita Vilkeviciute, Loresa Kriauciuniene, Greta Gedvilaite, Rasa Liutkeviciene
The receptor for advanced glycation end-product (RAGE) is a multi-ligand receptor involved in inflammation (13). The gene for RAGE is located on chromosome 6p21.3, and at least 30 polymorphisms have been identified till now. Most of the polymorphisms are rare coding changes or located in noncoding regions, including introns and the 5 ′ flanking region (13). Polymorphisms described in the promoter of RAGE gene, the − 374 T > A (rs1800624) and the − 429 T > C (rs1800625) polymorphisms were shown to have a marked effect on in vitro transcriptional activity. The − 429 C, − 374A and 63-bp del alleles resulted in an increase of gene expression of two-, three- and four-fold, respectively (14). Others studies state, that rs1800624 and rs1800625 polymorphisms, influences the transcriptional activity of RAGE promoter, act positively or negatively (15–17).
Possible effects of Porphyromonas gingivalis on the blood–brain barrier in Alzheimer’s disease
Published in Expert Review of Anti-infective Therapy, 2021
BBB dysfunction can cause accumulation of Aβ leading to alterations and disruption of the NVU (reviewed by [15]). The main transporter for efflux of accumulated Aβ at the BBB is low-density lipoprotein receptor-ligated protein 1 (LRP-1), while receptor for advanced glycation end product (RAGE) prevents Aβ from entering the brain [16,17]. With disability in LRP-1, BBB clearance is reduced, brain levels of Aβ are increased, and cognition is impaired [18]. Recently, LRP-1 was also found to regulate the uptake and spread of tau [19]. Increased levels of RAGE at the BBB can cause failing BBB function, which has been implicated as a main factor mediating Aβ cytotoxicity in AD [20]. Attenuation of RAGE may prevent Aβ from accumulating in the cerebral blood vessels and causing neurotoxicity [20].