Vitamin A (retinol) downregulates the receptor for advanced glycation endproducts (RAGE) by oxidant-dependent activation of p38 MAPK and NF-kB in human lung cancer A549 cells

Pasquali, Matheus Augusto de Bittencourt; Gelain, Daniel Pens; Zeidán-Chuliá, Fares; Pires, André Simões; Gasparotto, Juciano; Terra, Sílvia Resende; Moreira, José Cláudio Fonseca

doi:10.1016/j.cellsig.2013.01.013

Cited by 46 publications

(19 citation statements)

References 67 publications

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“…This evidence supports a causative role of oxidative stress in the toxic pattern exerted by QUIN, and prompts the design of antioxidant-based therapies against neurodegenerative events involving oxidative/excitotoxic/inflammatory components. Other groups have raised the relevance on the redox environment on the RAGE regulation, supporting the concept that this receptor functionally responds to oxidative conditions to favor different scenarios [70]. Up to this point, we have demonstrated, by different methodological means, that QUIN is able to induce RAGE up-regulation, and this effect can account for QUIN toxicity, leading to triggering inflammatory and degenerative pathways, as established in a previous report with the same model [11].…”

Section: Discussionmentioning

confidence: 99%

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

et al. 2015

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The receptor for advanced glycation end products (RAGE) is a pattern-recognition receptor involved in neurodegenerative and inflammatory disorders. RAGE induces cellular signaling upon binding to a variety of ligands. Evidence suggests that RAGE up-regulation is involved in quinolinate (QUIN)-induced toxicity. We investigated the QUIN-induced toxic events associated with early noxious responses, which might be linked to signaling cascades leading to cell death. The extent of early cellular damage caused by this receptor in the rat striatum was characterized by image processing methods. To document the direct interaction between QUIN and RAGE, we determined the binding constant (Kb) of RAGE (VC1 domain) with QUIN through a fluorescence assay. We modeled possible binding sites of QUIN to the VC1 domain for both rat and human RAGE. QUIN was found to bind at multiple sites to the VC1 dimer, each leading to particular mechanistic scenarios for the signaling evoked by QUIN binding, some of which directly alter RAGE oligomerization. This work contributes to the understanding of the phenomenon of RAGE-QUIN recognition, leading to the modulation of RAGE function.

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Section: Discussionmentioning

confidence: 99%

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

et al. 2015

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“…Researchers have shown that allantoin behaves as a potent antioxidant in its reactions with ROSs based on the experimental and theoretical results (Gus'kov and others ). There is increasing evidence that high levels of ROS could induce DNA damage‐mediated protein expression, NF‐κB activation and the downstream products IL‐1β which play an important role in the promotion and progression steps of cancer (Wang and others ; de Bittencourt Pasquali and others ). This suggests that Ginsenoside Rg3, CYF‐W, CYP‐W, CYF‐E, CYP‐E and allation prevent tumor growth by reducing the expression of pro‐inflammatory cytokines induced by oxidative stress.…”

Section: Resultsmentioning

confidence: 99%

Antioxidant and Antitumor Activities of the Extracts from Chinese Yam (Dioscorea opposite Thunb.) Flesh and Peel and the Effective Compounds

Liu

Fan

et al. 2016

Journal of Food Science

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The aims of this study are to investigate the antioxidant and antitumor activities of the water and ethanol extracts isolated from Chinese yam (Dioscorea opposite Thunb.) flesh (CYF) and peel (CYP) and the effective compounds. It was found that all peel portions have a better effect on reactive oxygen (ROS) scavenging assay than meat portions, especially for the water extract of Chinese yam peel (CYP-W). Its IC50 values for hydroxyl radical (OH•) scavenging assay (744.25 ± 3.46 μg/mL) and for 1,1-diphenyl-2-picrylhydrazyl scavenging assay (374.85 ± 6.78 μg/mL) were both lower than that of yam flesh (CYF-W). Furthermore, the antitumor property of yam peel was more effective than that of yam flesh (CYF-W) on mouse models, with tumor inhibition rates were 47.92% and 27.41% for Ehrlich Ascites Tumor (EAC) model and 40.44% and 24.22% for H22 hepatocarcinoma tumor (H22) model. Meanwhile, extracts of peel showed higher allantoin, total flavonoids, and total phenolics contents than extracts of flesh. In conclusion, this study demonstrated that CYP-W exerted better antitumor activity than flesh extracts and the scavenging ROS effects were also significantly higher in the CYP-W in vitro. Moreover, the data indicated that allantoin may play an important role on antioxidative and antitumor capacity in yam peel.

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“…These include antihypertensive drugs (Telmisartan [14] and Candesartan [15]), vitamin A [16], selenium [17], n-3 polyunsaturated fatty acids [18], antihyperlipidemic agents (statins) [19], antidiabetic agents (thiazolidinediones) [20], peroxisome proliferator-activated receptor gamma [21] and several extracts from Chinese traditional medicines, such as ginkgo biloba extract [22] and Panax notoginseng saponins (PNS) [23]. This suggests that reduced expression of RAGE may contribute to the therapeutic value of these drugs.…”

Section: Resultsmentioning

confidence: 99%

Hyperoside Downregulates the Receptor for Advanced Glycation End Products (RAGE) and Promotes Proliferation in ECV304 Cells via the c-Jun N-Terminal Kinases (JNK) Pathway Following Stimulation by Advanced Glycation End-Products In Vitro

Zhang

Sethiel

Shen

et al. 2013

IJMS

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Hyperoside is a major active constituent in many medicinal plants which are traditionally used in Chinese medicines for their neuroprotective, anti-inflammatory and antioxidative effects. The molecular mechanisms underlying these effects are unknown. In this study, quiescent ECV304 cells were treated in vitro with advanced glycation end products (AGEs) in the presence or absence of hyperoside. The results demonstrated that AGEs induced c-Jun N-terminal kinases (JNK) activation and apoptosis in ECV304 cells. Hyperoside inhibited these effects and promoted ECV304 cell proliferation. Furthermore, hyperoside significantly inhibited RAGE expression in AGE-stimulated ECV304 cells, whereas knockdown of RAGE inhibited AGE-induced JNK activation. These results suggested that AGEs may promote JNK activation, leading to viability inhibition of ECV304 cells via the RAGE signaling pathway. These effects could be inhibited by hyperoside. Our findings suggest a novel role for hyperoside in the treatment and prevention of diabetes.

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Vitamin A (retinol) downregulates the receptor for advanced glycation endproducts (RAGE) by oxidant-dependent activation of p38 MAPK and NF-kB in human lung cancer A549 cells

Cited by 46 publications

References 67 publications

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

Antioxidant and Antitumor Activities of the Extracts from Chinese Yam (Dioscorea opposite Thunb.) Flesh and Peel and the Effective Compounds

Hyperoside Downregulates the Receptor for Advanced Glycation End Products (RAGE) and Promotes Proliferation in ECV304 Cells via the c-Jun N-Terminal Kinases (JNK) Pathway Following Stimulation by Advanced Glycation End-Products In Vitro

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