Advanced glycation end-products disrupt human endothelial cells redox homeostasis: new insights into reactive oxygen species production

Dobi, Anthony; Bravo, Susana B.; Veeren, Bryan; Paradela-Dobarro, Beatriz; Álvarez, Ezequiel; Meilhac, Olivier; Viranaïcken, Wildriss; Baret, Pascal; Devin, Anne; Rondeau, Philippe

doi:10.1080/10715762.2018.1529866

Cited by 39 publications

(40 citation statements)

References 55 publications

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“…Furthermore, cells treated with AGEs showed an increase in basal oxygen consumption and proton leak as well as a reduction in the maximal respiration, spare respiration capacity, and non-mitochondrial respiration. This is in accordance with the tendency of AGEs to intensify proton leak, which is a sign of mitochondrial damage [72,76].…”

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermsupporting

confidence: 85%

“…ROS production was also reduced by myxothiazol, an inhibitor of complex III of the respiratory chain. These data support the role that NADPH oxidases and mitochondria play in the intracellular production of ROS mediated by AGEs [23,24,26,72,95,96]. Moreover, when cells were pretreated with anti-RAGE or soluble (sRAGE), the expression of NOX-1, NOX-2, and NOX-4 was inhibited and hence, ROS production [23,24,26,97], thus confirming the role of the AGE-RAGE axis in ROS generation by NADPH oxidases.…”

Section: Ages Produce Reactive Oxygen Species By a Nox-mediated Mechasupporting

confidence: 70%

“…Moreover, AGE production of ROS also enhances the expression [77] and the activities of antioxidant enzymes such as catalase, GPx, and SOD1, although no differences are described for the activity of SOD2. However, this increase in the antioxidant defenses appears to be depleted over time [72,78], which implies an indirect effect more than a transcriptional modulation.…”

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 97%

“…There is considerable evidence that ROS are generated upon interaction of AGEs with RAGE. Studies performed in endothelial cells [25,34,[49][50][51]72,73], macrophages [37], and cardiomyocytes [38] have identified an increase in the intracellular levels of H2O2, O2 − , and NO, as well as a higher release of H2O2 after treatment with AGEs by using redox fluorescence probes. Thus, the activation of the AGE-RAGE axis enhances oxidative AGE-RAGE interaction also results in an increased mRNA for heme oxygenase-1; it enhances the nuclear translocation of NF-κB, increases both the expression of VCAM-1 and endothelial permeability, and generates ROS by other mechanisms [25,[49][50][51].…”

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 99%

“…AGEs also produce oxidative modifications of proteins [79]. Thus, there is a production of intracellular advanced oxidation protein products (AOPPs) in endothelial cells [72] and macrophages [22] treated with AGEs.…”

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 99%

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Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases

et al. 2020

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Diets are currently characterized by elevated sugar intake, mainly due to the increased consumption of processed sweetened foods and drinks during the last 40 years. Diet is the main source of advanced glycation endproducts (AGEs). These are toxic compounds formed during the Maillard reaction, which takes place both in vivo, in tissues and fluids under physiological conditions, favored by sugar intake, and ex vivo during food preparation such as baking, cooking, frying or storage. Protein glycation occurs slowly and continuously through life, driving AGE accumulation in tissues during aging. For this reason, AGEs have been proposed as a risk factor in the pathogenesis of diet-related diseases such as diabetes, insulin resistance, cardiovascular diseases, kidney injury, and age-related and neurodegenerative diseases. AGEs are associated with an increase in oxidative stress since they mediate the production of reactive oxygen species (ROS), increasing the intracellular levels of hydrogen peroxide (H2O2), superoxide (O2−), and nitric oxide (NO). The interaction of AGEs with the receptor for AGEs (RAGE) enhances oxidative stress through ROS production by NADPH oxidases inside the mitochondria. This affects mitochondrial function and ultimately influences cell metabolism under various pathological conditions. This short review will summarize all evidence that relates AGEs and ROS production, their relationship with diet-related diseases, as well as the latest research about the use of natural compounds with antioxidant properties to prevent the harmful effects of AGEs on health.

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Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermsupporting

confidence: 85%

Section: Ages Produce Reactive Oxygen Species By a Nox-mediated Mechasupporting

confidence: 70%

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 97%

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 99%

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 99%

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Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases

et al. 2020

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Structural and functional connectivity alteration patterns of the cingulate gyrus in Type 2 diabetes

Zhang,

Huang,

Liu

et al. 2023

Ann Clin Transl Neurol

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ObjectiveWe aimed to reveal the role of structural and functional alterations of cingulate gyrus in early cognitive impairment in Type 2 diabetes mellitus (T2DM) patients.MethodsFifty‐six T2DM patients and 60 healthy controls (HCs) underwent a neuropsychological assessment and sagittal three‐dimensional T1‐weighted and resting‐state functional MRI. Differences in the cortical thickness of the cingulate cortex and the functional connectivity (FC) of the nine subregions of the cingulate gyrus and the whole brain were compared between T2DM patients and HCs. Correlation analysis was performed between cortex thickness and FC and the participants' clinical/cognitive variables.ResultsThe cortical thickness of the cingulate gyrus was not significantly different between T2DM patients and HCs. However, the T2DM patients showed significantly lower FC between the pregenual ACC (pACC) and the bilateral hippocampus, significantly higher FC between the pACC and bilateral lateral prefrontal cortex (LPFC) and left precentral gyrus, and significantly lower FC between the retrosplenial cortex (RSC) and right cerebellar Crus I. The FC between the pACC and the left hippocampus was negatively correlated with the FC between the pACC and LPFC (r = −0.306, p = 0.022).InterpretationThe pACC and the RSC show dysfunctional connectivity before the appearance of structural abnormalities in T2DM patients. Abnormal FC of the pACC with the bilateral hippocampus and LPFC may imply a neural compensatory mechanism for memory function. These findings provide valuable information and new directions for possible interventions for the T2DM‐related cognitive impairment.

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Distribution of microglia/immune cells in the brain of adult zebrafish in homeostatic and regenerative conditions: Focus on oxidative stress during brain repair

Narra

Rondeau

Fernezelian

et al. 2022

J of Comparative Neurology

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Microglia are macrophage‐like cells exerting determinant roles in neuroinflammatory and oxidative stress processes during brain regeneration. We used zebrafish as a model of brain plasticity and repair. First, by performing L‐plastin (Lcp1) immunohistochemistry and using transgenic Tg(mpeg1.1:GFP) or Tg(mpeg1.1:mCherry) fish, we analyzed the distribution of microglia/immune cells in the whole brain. Specific regional differences were evidenced in terms of microglia/immune cell density and morphology (elongated, branched, highly branched, and amoeboid). Taking advantage of Tg(fli:GFP) and Tg(GFAP::GFP) enabling the detection of endothelial cells and neural stem cells (NSCs), we highlighted the association of elongated microglia/immune cells with blood vessels and rounded/amoeboid microglia with NSCs. Second, after telencephalic injury, we showed that L‐plastin cells were still abundantly present at 5 days post‐lesion (dpl) and were associated with regenerative neurogenesis. Finally, RNA‐sequencing analysis from injured telencephalon (5 dpl) confirmed the upregulation of microglia/immune cell markers and highlighted a significant increase of genes involved in oxidative stress (nox2, nrf2a, and gsr). The analysis of antioxidant activities at 5 dpl also revealed an upregulation of superoxide dismutase and persistent H2O2 generation in the injured telencephalon. Also, microglia/immune cells were shown to be a source of oxidative stress at 5 dpl. Overall, our data provide a better characterization of microglia/immune cell distribution in the healthy zebrafish brain, highlighting some evolutionarily conserved features with mammals. They also emphasize that 5 days after injury, microglia/immune cells are still activated and are associated to a persistent redox imbalance. Together, these data raise the question of the role of oxidative stress in regenerative neurogenesis in zebrafish.

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Advanced glycation end-products disrupt human endothelial cells redox homeostasis: new insights into reactive oxygen species production

Cited by 39 publications

References 55 publications

Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases

Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases

Structural and functional connectivity alteration patterns of the cingulate gyrus in Type 2 diabetes

Distribution of microglia/immune cells in the brain of adult zebrafish in homeostatic and regenerative conditions: Focus on oxidative stress during brain repair

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