Central role of RAGE-dependent neointimal expansion in arterial restenosis

Sakaguchi, Taichi; Yan, Shi Fang; Yan, Shi Du; Белов, Д. В.; Rong, Ling; Sousa, Mónica Mendes; Andrassy, Martin; Marso, Steven P.; Duda, Stephan H.; Arnold, Bernd; Liliensiek, Birgit; Nawroth, Peter P.; Stern, David M.; Schmidt, Ann Marie; Naka, Yoshifumi

doi:10.1172/jci17115

Cited by 181 publications

(210 citation statements)

References 69 publications

Supporting

Mentioning

206

Contrasting

Order By: Relevance

“…Administration of sRAGE, a decoy of RAGE, can reduce injury-associated, RAGE signal-mediated chronic inflammation and minimize maladaptation and remodeling in vasculature, thus decreasing the risk of cardiovascular diseases and other vessel-associated complications. Although previous studies discovered that sRAGE can be used to block neointimal growth and formation of atherosclerotic plaques in animal models, to achieve the blockage, a high dose and multiple administrations of sRAGE produced in insect Sf9 cells were employed [17], [18], [19], [26], [27]. Our recent study 21 demonstrated that specific N-glycoform modifications are the key determinant underlying sRAGE bioactivity and therapeutic efficacy: a low, single dose of sRAGE produced in CHO cells can significantly reduce injury-associated inflammation and neointimal growth.…”

Section: Discussionmentioning

confidence: 99%

“…Although previous studies assessed how sRAGE treatment affected neointimal growth via histomorphologic analyses of postmortem vessel sections,[17], [18], [21] direct assessment of sRAGE action in vivo has not been performed. Vessel ultrasound sonography is a technique that can be used noninvasively in clinical practice to monitor arterial structure and function [23], [24], [25].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vessel Ultrasound Sonographic Assessment of Soluble Receptor for Advanced Glycation End Products Efficacy in a Rat Balloon Injury Model

Tae¹,

Petrashevskaya²,

Ahmet³

et al. 2014

Current Therapeutic Research

View full text Add to dashboard Cite

ObjectiveWe aimed to assess the therapeutic efficacy of differentially modified soluble receptor for advanced glycation end products (sRAGE) in vivo using vessel ultrasound sonography and to compare the sonography data with those from postmortem histomorphologic analyses to have a practical reference for future clinical applications.MethodsVessel ultrasound sonography was performed in a sRAGE-treated rat carotid artery balloon injury model at different time points after the surgery, and therapeutic efficacy of different doses of sRAGE produced in Chinese hamster ovary cells and with different N-glycoform modifications were assessed.ResultsVessel ultrasound sonography found that sRAGE produced in Chinese hamster ovary cells with complex N-glycoform modifications is highly effective, and is consistent with our recent findings in the same model assessed with histology. We also found that sonography is less sensitive than histology when a higher dose of sRAGE is administered.ConclusionsSonograph results are consistent with those obtained from histology; that is, sRAGE produced in Chinese hamster ovary cells has significantly higher efficacy than insect cell-originated sRAGE cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vessel Ultrasound Sonographic Assessment of Soluble Receptor for Advanced Glycation End Products Efficacy in a Rat Balloon Injury Model

Tae¹,

Petrashevskaya²,

Ahmet³

et al. 2014

Current Therapeutic Research

View full text Add to dashboard Cite

show abstract

“…It has been demonstrated that wild-type mice undergoing arterial endothelial denudation displayed striking up-regulation of advanced glycation end products (AGEs) and the receptor for advanced glycation end products (RAGE) in the injured vessel, particularly in activated smooth muscle cells of the expanding neointima [1,2,3]. AGEs can cause vascular damage through several mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Cariporide, a Specific Na<sup>+</sup>/H<sup>+</sup> Exchanger 1 Blocker, Inhibits Neointimal Proliferation Induced by Advanced Glycation End Products in a Balloon Injury Rat Model

Wu¹,

Yang

Liu

et al. 2013

Pharmacology

View full text Add to dashboard Cite

Aims: The association between diabetes and neointimal expansion after vascular injury has been attributed to the accumulation of advanced glycation end products (AGEs). Here we investigated the inhibitory effect of cariporide, a specific Na⁺/H⁺ exchanger 1 blocker, on neointimal proliferation induced by AGEs in a balloon injury model. Methods: Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP) was monitored by reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. The level of reactive oxygen species (ROS) was determined by specific fluorescent probe. The phosphorylation of the nuclear factor-ĸB (NF-ĸB) system was studied by Western blot. Results: Cariporide significantly suppressed AGE-induced neointimal hyperplasia, vascular smooth muscle cell (VSMC) proliferation, COX-2, MMP-2 and MMP-9 expression. In addition, cariporide decreased AGE-induced ROS, malondiadehyde level and increased the superoxide dismutase and glutathione peroxidase activity. We also found that cariporide blocked AGE-induced NF-ĸB activation and inhibitor-ĸB degradation. Conclusions: The results indicated that cariporide inhibited AGE-induced neointimal formation by suppressing the VSMC proliferation and the up-regulation of COX-2, MMP-2, MMP-9 via inhibiting ROS and NF-ĸB activation.

show abstract

“…ctRAGE has been shown to be a pivotal element required for RAGE ligand-stimulated cellular responses in multiple studies [27-29]. In addition, RAGE-dependent signal transduction requires the interaction between the ctRAGE and mDia1 that has been identified as a binding partner of the cytoplasmic domain.…”

Section: Discussionmentioning

confidence: 99%

Mdia1 is Crucial for Advanced Glycation End Product-Induced Endothelial Hyperpermeability

Zhou

Weng

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Disruption of endothelial barrier integrity in response to advanced glycation end products (AEGs) stimulation contributes to vasculopathy associated with diabetes mellitus. Mammalian diaphanous-related formin (mDia1) has been reported to bind to the cytoplasmic domain of the receptor for advanced glycation end products (RAGE), which induces a series of cellular processes. This study directly evaluated the participation of mDia1 in AGE-induced hyperpermeability and revealed the precise intracellular signal transductions of this pathological process. Methods: Human umbilical vein endothelial cells (HUVECs) were used in the in vitro studies. Trans-endothelial electric resistance and permeability coefficient for dextran (Pd) were measured to analyze cell permeability. Western blotting, immunofluorescence staining and flow cytometry assay were performed to investigate the underlying mechanism. Dextran flux across the mesentery in mice was monitored to investigate in vivo microvascular permeability. Results: we found that AGEs evoked Nox4 membrane translocation, reactive oxygen species production, phosphorylation of Src and VE-cadherin, dissociation of adherens junctions and eventual endothelial hyperpermeability through RAGE-mDia1 binding. Cells overexpressing mDia1 by recombinant adenovirus infection showed stronger cellular responses induced by AGEs. Down-regulation of mDia1 by infection with an adenovirus encoding siRNA or blockade of RAGE-mDia1 binding by transfection with RAGE mutant plasmids into HUVECs abolished these AGE-induced effects. Furthermore, knockdown of mDia1 using an adenovirus or genetical knockout of RAGE in C57 mice rescued AGE-evoked microvascular hyperpermeability. Conclusion: Our study revealed that mDia1 plays a critical role in AGE-induced microvascular hyperpermeability through binding to RAGE.

show abstract

Central role of RAGE-dependent neointimal expansion in arterial restenosis

Cited by 181 publications

References 69 publications

Vessel Ultrasound Sonographic Assessment of Soluble Receptor for Advanced Glycation End Products Efficacy in a Rat Balloon Injury Model

Vessel Ultrasound Sonographic Assessment of Soluble Receptor for Advanced Glycation End Products Efficacy in a Rat Balloon Injury Model

Cariporide, a Specific Na<sup>+</sup>/H<sup>+</sup> Exchanger 1 Blocker, Inhibits Neointimal Proliferation Induced by Advanced Glycation End Products in a Balloon Injury Rat Model

Mdia1 is Crucial for Advanced Glycation End Product-Induced Endothelial Hyperpermeability

Contact Info

Product

Resources

About