Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium
DC Field | Value | Language |
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dc.contributor.author | Nam, Mi-Hyun | - |
dc.contributor.author | Son, Won-Rak | - |
dc.contributor.author | Lee, Young Sik | - |
dc.contributor.author | Lee, Kwang-Won | - |
dc.date.accessioned | 2021-09-05T00:58:27Z | - |
dc.date.available | 2021-09-05T00:58:27Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2015 | - |
dc.identifier.issn | 1541-9061 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/96220 | - |
dc.description.abstract | Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-a and interleukin-1 beta via extracellular-signal-regulated kinases phosphorylation and nuclear factor-jB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | TAYLOR & FRANCIS INC | - |
dc.subject | NF-KAPPA-B | - |
dc.subject | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | - |
dc.subject | INHIBITOR TYPE-I | - |
dc.subject | MATRIX-METALLOPROTEINASE-9 EXPRESSION | - |
dc.subject | NADPH OXIDASE | - |
dc.subject | PROLIFERATION | - |
dc.subject | ATHEROSCLEROSIS | - |
dc.subject | ACTIVATION | - |
dc.subject | INFLAMMATION | - |
dc.subject | MIGRATION | - |
dc.title | Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Young Sik | - |
dc.contributor.affiliatedAuthor | Lee, Kwang-Won | - |
dc.identifier.doi | 10.1080/15419061.2016.1225196 | - |
dc.identifier.scopusid | 2-s2.0-84986205401 | - |
dc.identifier.wosid | 000389751300004 | - |
dc.identifier.bibliographicCitation | CELL COMMUNICATION AND ADHESION, v.22, no.2-6, pp.67 - 78 | - |
dc.relation.isPartOf | CELL COMMUNICATION AND ADHESION | - |
dc.citation.title | CELL COMMUNICATION AND ADHESION | - |
dc.citation.volume | 22 | - |
dc.citation.number | 2-6 | - |
dc.citation.startPage | 67 | - |
dc.citation.endPage | 78 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | - |
dc.subject.keywordPlus | INHIBITOR TYPE-I | - |
dc.subject.keywordPlus | MATRIX-METALLOPROTEINASE-9 EXPRESSION | - |
dc.subject.keywordPlus | NADPH OXIDASE | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | ATHEROSCLEROSIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordAuthor | Advanced glycation end-products | - |
dc.subject.keywordAuthor | inflammatory cytokines | - |
dc.subject.keywordAuthor | reactive oxygen species | - |
dc.subject.keywordAuthor | vascular dysfunction | - |
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