Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Nam, Mi Hyun; Son, Weon-Young; Lee, Young Sik; Lee, Kwang Won

doi:10.1080/15419061.2016.1225196

Cited by 28 publications

(15 citation statements)

References 45 publications

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“…It has been described that AGEs can produce ROS by activating NADPH oxidases [67,68], the mitochondrial respiratory chain, microsomal enzymes, xanthine oxidase, and arachidonic acid pathways [69][70][71] by interacting with their receptor ( Figure 2). There is considerable evidence that ROS are generated upon interaction of AGEs with RAGE.…”

Section: Reactive Oxygen Species/reactive Nitrogen Species Are Intermmentioning

confidence: 99%

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 Intermmentioning

confidence: 99%

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

et al. 2020

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“…In particular, PM purified from P. asiatica is a phenylpropanoid glycoside that contains caffeic acid derivatives [31, 33]; nevertheless, the molecular mechanism of how PM modulates endothelial dysfunction remains uncertain. Our groups have reported that glycolaldehyde-derived AGEs stimulated intracellular ROS production and pro-inflammatory mediators including TNF-α and IL-1β via the AGE-RAGE axis [39]. One recent study showed that co-treatment with PM and glycer-AGEs in keratinocytes and fibroblasts inhibits UVB-irradiation- and AGE-induced RAGE overexpression and proinflammatory cytokine expression via attenuating MAPK activation by ROS [40].…”

Section: Discussionmentioning

confidence: 99%

Plantamajoside from Plantago asiatica modulates human umbilical vein endothelial cell dysfunction by glyceraldehyde-induced AGEs via MAPK/NF-κB

Son

Nam

Hong

et al. 2017

BMC Complement Altern Med

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Background Plantago asiatica has been traditionally used for traditional medicine around East Asia. Plantamajoside (PM), which is isolated from this plant, is known for biological properties including anti-inflammation and antioxidant activity. To demonstrate the biological activity of PM against endothelial dysfunction induced by advanced glycation end-products (AGEs), a cellular inflammatory mechanism system was evaluated in human umbilical vein endothelial cells (HUVECs).MethodsWe obtained PM through previous research in our laboratory. We formed the AGEs from bovine serum albumin with glyceraldehyde in the dark for seven days. To confirm the modulation of the inflammatory mechanism in endothelial dysfunction, we quantified the various pro-inflammatory cytokines and endothelial dysfunction-related proteins in the HUVECs with Western blotting and with real-time and quantitative real-time polymerase chain reactions.ResultsCo-treatment with PM and AGEs significantly suppressed inflammatory cytokines and adhesion molecule expression. Moreover, the PM treatment for down-regulated inflammatory signals and blocked monocyte adhesion on the HUVECs.ConclusionsTheses results demonstrated that PM, as a potential natural compound, protects AGE-induced endothelial cells against inflammatory cellular dysfunction.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1570-1) contains supplementary material, which is available to authorized users.

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“…It is well accepted that overexpression of RAGE is activated by AGEs in vascular dysfunction and resulting in apoptosis, oxidative stress and inflammation responses (35). There is a growing body of evidence that shows that AGE-RAGE interaction with a positive feedback loop is related to the dysfunction of VSMCs (10,36–38). A previous study found that 100 µ g/ml AGEs enhanced vascular calcification through a RAGE/oxidative stress pathway (38).…”

Section: Discussionmentioning

confidence: 99%

Advanced glycation end products promote the proliferation and migration of primary rat vascular smooth muscle cells via the upregulation of BAG3

et al. 2017

International Journal of Molecular Medicine

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The present study was aimed to investigate the role of reactive oxygen species (ROS) on advanced glycation end product (AGE)-induced proliferation and migration of vascular smooth muscle cells (VSMCs) and whether Bcl-2-associated athanogene 3 (BAG3) is involved in the process. Primary rat VSMCs were extracted and cultured in vitro. Cell viability was detected by MTT assay and cell proliferation was detected by EdU incorporation assay. Cell migration was detected by wound healing and Transwell assays. BAG3 was detected using qPCR and western blot analysis. Transcriptional and translational inhibitors (actinomycin D and cycloheximide, respectively) were used to study the effect of AGEs on the expression of BAG3 in VSMCs. Lentiviral plasmids containing short hairpin RNA (shRNA) against rat BAG3 or control shRNA were transduced into VSMCs. Cellular ROS were detected by 2′,7′-dichlorofluorescein diacetate (DCFH-DA) staining. Mitochondrial membrane potential was detected by tetramethylrhodamine methyl ester (TMRE) staining. AGEs significantly increased the expression of BAG3 in a dose-and time-dependent manner. Furthermore, AGEs mainly increased the expression of BAG3 mRNA by increasing the RNA synthesis rather than inhibiting the RNA translation. BAG3 knockdown reduced the proliferation and migration of VSMCs induced by AGEs. BAG3 knockdown reduced the generation of ROS and sustained the mitochondrial membrane potential of VSMCs. Reduction of ROS production by N-acetylcysteine (NAC), a potent antioxidant, also reduced the proliferation and migration of VSMCs. On the whole, the present study demonstrated for the first time that AGEs could increase ROS production and promote the proliferation and migration of VSMCs by upregulating BAG3 expression. This study indicated that BAG3 should be considered as a potential target for the prevention and/or treatment of vascular complications of diabetes.

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Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Cited by 28 publications

References 45 publications

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

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

Plantamajoside from Plantago asiatica modulates human umbilical vein endothelial cell dysfunction by glyceraldehyde-induced AGEs via MAPK/NF-κB

Advanced glycation end products promote the proliferation and migration of primary rat vascular smooth muscle cells via the upregulation of BAG3

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