Cutaneous activation of rage in nonsystemic vasculitic and diabetic neuropathy

Bekircan-Kurt, Can Ebru; Üçeyler, Nurcan; Sommer, Claudia

doi:10.1002/mus.24164

Cited by 16 publications

(17 citation statements)

References 28 publications

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“…More detailed studies aimed at deciphering the molecular mechanisms by which RAGE exerts its actions in DPN progression, conducted in RAGE-deficient mice after acute peripheral nerve injury, revealed that RAGE, in addition to triggering a cascade of detrimental metabolic changes, contributes to nerve pathology by promoting a switch in macrophage phenotype from anti-inflammatory to proinflammatory at the injury site (Juranek et al, 2013a). Two other recent studies focused on the prognostic measurement and correlation between AGE and RAGE expression in skin biopsies and neurological scores on diabetic neuropathy severity scale in diabetic patients revealed that there is a significant increase in skin biopsy AGE and RAGE levels, which is strongly correlated with neuropathy severity, thus further supporting the role of RAGE in the pathogenesis of this disease (Bekircan-Kurt et al, 2014;Park et al, 2014).…”

Section: Rage In Peripheral Neuropathiesmentioning

confidence: 88%

Receptor for advanced glycation end-products in neurodegenerative diseases

Juranek¹,

Ray²,

Banach

et al. 2015

Reviews in the Neurosciences

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AbstractThis review, for the first time, aims to summarize the current knowledge in the emerging field of RAGE (receptor for advanced glycation end-products) studies in neurodegeneration and neurodegenerative diseases. RAGE, a member of the multiligand cell surface immunoglobulin family, has been implicated in numerous pathological conditions – from diabetes and cardiovascular diseases to tumors and neurodegenerative disorders, such as Alzheimer’s disease, familial amyloid polyneuropathy, diabetic neuropathy, Parkinson’s disease, and Huntington’s disease. Until now, the detailed mechanisms of the contribution of RAGE to neurodegeneration remain elusive; however, mounting evidence suggests that its detrimental actions are triggered by its ligand interactions and contribute to increased neuroinflammation, neuronal degeneration, and apoptosis. Deciphering the role of RAGE in neurodegenerative disorders will be a milestone in our basic understanding of the mechanisms involved in the pathogenesis of neurodegeneration, helping to delineate molecular links between complex RAGE signaling pathways and neuronal dysfunction and neurodegeneration.

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Section: Rage In Peripheral Neuropathiesmentioning

confidence: 88%

Receptor for advanced glycation end-products in neurodegenerative diseases

Juranek¹,

Ray²,

Banach

et al. 2015

Reviews in the Neurosciences

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“…Increased advanced glycation endproducts and RAGE have been described in dermal microvessels and T cells of patients with NSVN; however patients with diabetic neuropathy had similar expression to NSVN patients relative to healthy controls [8], suggesting that this may be a marker of vasculopathy. Another study designed to deduce whether apoptosis played a role in endothelial cell injury in 19 patients with vasculitic neuropathy by immunohistochemistry and terminal deoxynucleotidyl transferase-mediated nick end labeling demonstrated expression of granzyme A, granzyme B and T-cell restricted intracellular antigen, as well as Fas and FasL on epineurial perivascular mononuclear cells by immunohistochemistry, implying that T-lymphocyte and macrophage apoptosis may occur during a phase of peripheral nerve recovery in this disorder [46].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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“…AGE measurement can in fact be made in plasma [ 26 – 30 ], in urine [ 26 ], or in tissues, skin being the most often used tissue [ 31 , 32 ]. Among several compounds already studied, CML is the best characterized AGE [ 29 ] and the most consistently assessed one in plasma analysis [ 26 – 30 ].…”

Section: Discussionmentioning

confidence: 99%

Advanced Glycation End Products Evolution after Pancreas‐Kidney Transplantation: Plasmatic and Cutaneous Assessments

Martins

Oliveira

Vizcaíno

et al. 2016

Oxidative Medicine and Cellular Longevity

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Diabetes mellitus leads to increased Advanced Glycation End Products (AGE) production, which has been associated with secondary diabetic complications. Type 1 diabetic patients undergoing pancreas-kidney transplantation (SPKT) can restore normoglycemia and renal function, eventually decreasing AGE accumulation. We aimed to prospectively study AGE evolution after SPKT. Circulating AGE were assessed in 20 patients, at time 0 (T0), 3 months (T3), 6 months (T6), and 12 months (T12) after successful SPKT. Global AGE and carboxymethyllysine (CML) were analyzed, as well as advanced oxidation protein products (AOPP). Skin biopsies were obtained at T0 and T12. Immunohistochemistry with anti-AGE antibody evaluated skin AGE deposition. AGE mean values were 16.8 ± 6.4 μg/mL at T0; 17.1 ± 3.8 μg/mL at T3; 17.5 ± 5.6 μg/mL at T6; and 16.0 ± 5.2 μg/mL at T12. CML mean values were 0.94 ± 0.36 ng/mL at T0; 1.11 ± 0.48 ng/mL at T3; 0.99 ± 0.42 ng/mL at T6; and 0.78 ± 0.38 ng/mL at T12. AOPP mean values were 130.1 ± 76.8 μMol/L at T0; 137.3 ± 110.6 μMol/L at T3; 116.4 ± 51.2 μMol/L at T6; and 106.4 ± 57.9 μMol/L at T12. CML variation was significant (P = 0.022); AOPP variation was nearly significant (P = 0.076). Skin biopsies evolved mostly from a cytoplasmic diffuse to a peripheral interkeratinocytic immunoreaction pattern; in 7 cases, a reduction in AGE immunoreaction intensity was evident at T12. In conclusion, glycoxidation markers decrease, plasmatic and on tissues, may start early after SPKT. Studies with prolonged follow-up may confirm these data.

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Cutaneous activation of rage in nonsystemic vasculitic and diabetic neuropathy

Abstract: Dermal RAGE is increased in NSVN and DN, supporting the concept of a role of the RAGE pathway in the pathophysiology of dermal inflammation and skin denervation in NSVN and DN.

Cited by 16 publications

References 28 publications

Receptor for advanced glycation end-products in neurodegenerative diseases

Receptor for advanced glycation end-products in neurodegenerative diseases

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Advanced Glycation End Products Evolution after Pancreas‐Kidney Transplantation: Plasmatic and Cutaneous Assessments

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