Receptor for Advanced Glycation End Products (RAGE) Prevents Endothelial Cell Membrane Resealing and Regulates F-actin Remodeling in a β-Catenin-dependent Manner

Xiong, Fei; Leonov, Sergey; Howard, Amber Cyan; Xiong, Shanbai; Zhang, Bin; Mei, Lin; McNeil, Paul L.; Simon, Sylvia; Xiong, Wen Cheng

doi:10.1074/jbc.m111.261073

Cited by 34 publications

(29 citation statements)

References 42 publications

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“…Treatment with either FPS‐ZM1 or RAP not only attenuated TDI‐induced airway inflammation and hyperresponsiveness but also reduced total, cytoplasmic and nuclear levels of β‐catenin, enhanced β‐catenin phosphorylation at Ser 33 / 37 /Thr 41 , which triggers ubiquitination, down‐regulated expression of β‐catenin targeted genes, and tended to keep β‐catenin at the cytomembrane, shifting β‐catenin from a signalling active pattern to an adhesive function. This was in agreement with what was found in endothelial cells (Xiong et al , ), but in disagreement with the data of Li et al . in osteoblastic cells, where there was a reduction of total β‐catenin level in response to Wnt3a‐CM after RAGE overexpression (Li et al , ).…”

Section: Discussionsupporting

confidence: 89%

The receptor for advanced glycation end products is required for β‐catenin stabilization in a chemical‐induced asthma model

Yao

Zhao

Tang

et al. 2016

British J Pharmacology

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*These authors made equal contributions to this paper. BACKGROUND AND PURPOSECytoplasmic retention of β-catenin will lead to its nuclear translocation and subsequent interaction with the transcription factor TCF/LEF that regulates target gene expression. We have previously demonstrated aberrant expression of β-catenin in a model of asthma induced by toluene diisocyanate (TDI). The aim of this study was to examine whether the receptor for advanced glycation end products (RAGE) can regulate β-catenin expression in TDI-induced asthma. EXPERIMENTAL APPROACHMale BALB/c mice were sensitized and challenged with TDI to generate a chemically-induced asthma model. Inhibitors of RAGE, FPS-ZM1 and the RAGE antagonist peptide (RAP), were injected i.p. after each challenge. Airway resistance was measured in vivo and bronchoalveolar lavage fluid was analysed. Lungs were examined by histology and immunohistochemistry. Western blotting and quantitative PCR were also used. KEY RESULTSExpression of RAGE and of its ligands HMGB1, S100A12, S100B, HSP70 was increased in TDI-exposed lungs. These increases were inhibited by FPS-ZM1 or RAP. Either antagonist blunted airway reactivity, airway inflammation and goblet cell metaplasia, and decreased release of Th2 cytokines. TDI exposure decreased level of membrane β-catenin, phosphorylated Akt (Ser 473 ), inactivated GSK3β (Ser 9 ), dephosphorylated β-catenin at Ser 33 / 37 /Thr 41 , which controls its cytoplasmic degradation, increased phosphorylated β-catenin at Ser 552 , raised cytoplasmic and nuclear levels of β-catenin and up-regulated its targeted gene expression (MMP2, MMP7, MMP9, VEGF, cyclin D1, fibronectin), all of which were reversed by RAGE inhibition. CONCLUSION AND IMPLICATIONSRAGE was required for stabilization of β-catenin in TDI-induced asthma, identifying protective effects of RAGE blockade in this model. AbbreviationsBALF, bronchoalveolar lavage fluid; GSK, glycogen synthase kinase; RAGE, receptor for advanced glycation end products; TDI, toluene diisocyanate

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Section: Discussionsupporting

confidence: 89%

The receptor for advanced glycation end products is required for β‐catenin stabilization in a chemical‐induced asthma model

Yao

Zhao

Tang

et al. 2016

British J Pharmacology

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“…RAGE has been proposed to serve as a primary receptor for S100 proteins in the extracellular space, and plays an important role in S100A8- or S100A9-induced proliferation and migration of prostate and breast and colon cancer cells involving the MAPK/NF-κB signaling [18]–[20], [56], [70]–[71]. RAGE has been reported to increase the β-catenin level in human umbilical vein endothelial cell line (ECV–304) [72]. In addition, MAPK pathways have been shown to have unique and provocative roles that impact the Wnt/β-catenin signaling [73]-[76].…”

Section: Discussionmentioning

confidence: 99%

S100A8 and S100A9 Are Associated with Colorectal Carcinoma Progression and Contribute to Colorectal Carcinoma Cell Survival and Migration via Wnt/β-Catenin Pathway

Duan

et al. 2013

PLoS ONE

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Background and ObjectiveS100A8 and S100A9, two members of the S100 protein family, have been reported in association with the tumor cell differentiation and tumor progression. Previous study has showed that their expression in stromal cells of colorectal carcinoma (CRC) is associated with tumor size. Here, we investigated the clinical significances of S100A8 and S100A9 in tumor cells of CRC and their underlying molecular mechanisms.MethodsExpression of S100A8 and S100A9 in colorectal carcinoma and matching distal normal tissues were measured by reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry and western blot. CRC cell lines treated with the recombinant S100A8 and S100A9 proteins were used to analyze the roles and molecular mechanisms of the two proteins in CRC in vitro.ResultsS100A8 and S100A9 were elevated in more than 50% of CRC tissues and their expression in tumor cells was associated with differentiation, Dukes stage and lymph node metastasis. The CRC cell lines treatment with recombinant S100A8 and S100A9 proteins promoted the viability and migration of CRC cells. Furthermore, the two recombinant proteins also resulted in the increased levels of β-catenin and its target genes c-myc and MMP7. β-catenin over-expression in CRC cells by Adβ-catenin increased cell viability and migration. β-catenin knock-down by Adsiβ-catenin reduced cell viability and migration. Furthermore, β-catenin knockdown also partially abolished the promotive effects of recombinant S100A8 and S100A9 proteins on the viability and migration of CRC cells.ConclusionsOur work demonstrated that S100A8 and S100A9 are linked to the CRC progression, and one of the underlying molecular mechanisms is that extracellular S100A8 and S100A9 proteins contribute to colorectal carcinoma cell survival and migration via Wnt/β-catenin pathway.

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“…Furthermore, induced levels of vasoconstrictor mediator endothelin-1 were induced to block Aβ-associated suppressed cerebral blood flow. A recent study by Xiong et al [165] reported that RAGE expression in human umbilical vein endothelial cell line (ECV-304) had prevented the endothelial cell membrane repair by activating β-catenin levels that resulted in reduced F-actin stress fibres and attenuated plasma membrane resealing [165]. Impaired glucose metabolism also plays a very important role in NFTs formation by promoting hyperphosphorylation of tau protein.…”

Section: Abnormal Glucose Metabolismmentioning

confidence: 97%

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

Ahmad

2012

Mol Neurobiol

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Alzheimer's disease (AD) and diabetes are among the most common diseases associated with ageing. The pathology of AD is strongly associated with accumulated misfolding proteins that results in neuronal dysfunction within the brain. Diabetes, on the contrary, is characterised by altered insulin signaling that results in reduced glucose uptake, metabolic suppression of energy consuming cells and conversion of glucose to fat in the liver. Despite distinguishing features, these diseases share common elements and may in fact be viewed as fundamentally similar disorders that differ in magnitude of specific traits, primarily affected tissues and time of onset. In this review, we outline the fundamental basis of each of the two diseases and highlight similarities in their pathophysiology. Further ahead we will discuss these features in relation to the development of drugs to treat these two diseases, particularly AD, for which the development of therapeutic chemicals has proven to be particularly difficult. We conclude with comments on efforts to develop a simple organism, Caenorhabditis elegans, as a genetic model to be used to study the systems biology of diabetes and AD.

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Receptor for Advanced Glycation End Products (RAGE) Prevents Endothelial Cell Membrane Resealing and Regulates F-actin Remodeling in a β-Catenin-dependent Manner

Cited by 34 publications

References 42 publications

The receptor for advanced glycation end products is required for β‐catenin stabilization in a chemical‐induced asthma model

The receptor for advanced glycation end products is required for β‐catenin stabilization in a chemical‐induced asthma model

S100A8 and S100A9 Are Associated with Colorectal Carcinoma Progression and Contribute to Colorectal Carcinoma Cell Survival and Migration via Wnt/β-Catenin Pathway

Overlapped Metabolic and Therapeutic Links between Alzheimer and Diabetes

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