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  1. NTU Scholars
  2. 醫學院
  3. 醫學系
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/593856
DC FieldValueLanguage
dc.contributor.authorChen, Ying-Juen_US
dc.contributor.authorDING-CHENG CHANen_US
dc.contributor.authorCHIH-KANG CHIANGen_US
dc.contributor.authorCHING-CHIA WANGen_US
dc.contributor.authorYang, Ting-Huaen_US
dc.contributor.authorLan, Kuo-Chengen_US
dc.contributor.authorSUNG-CHUAN CHAOen_US
dc.contributor.authorKEH-SUNG TSAIen_US
dc.contributor.authorRONG-SEN YANGen_US
dc.contributor.authorLiu, Shing-Hwaen_US
dc.date.accessioned2022-02-08T03:47:18Z-
dc.date.available2022-02-08T03:47:18Z-
dc.date.issued2016-05-
dc.identifier.issn0736-0266-
dc.identifier.urihttps://scholars.lib.ntu.edu.tw/handle/123456789/593856-
dc.description.abstractAging and diabetes are known to be the major cause to affect the progression of osteoarthritis (OA). Advanced glycation end products (AGEs) have been observed to accumulate in various organs especially in joint tissue and do damage to the joint tissue during aging and diabetes. Synovial angiogenesis and inflammation are observed across the full range of OA severity. The signaling pathway of AGEs on vascular endothelial growth factor (VEGF) production and inflammatory responses in synoviocytes are still unclear. Here, we investigated the role of receptor for AGEs (RAGE) and the signaling pathway involved in AGEs-induced VEGF production and inflammatory responses in human synoviocytes. Human synoviocytes were cultured and treated with AGEs (25-100 µg/ml). AGEs significantly induced the protein expressions of cyclooxygenase-2 (COX-2) and VEGF and the productions of prostaglandin-E2 (PGE2), VEGF, interleukin-6 (IL-6), and metalloproteinase-13 (MMP-13) in human synoviocytes in a dose-dependent manner. Moreover, AGEs markedly activated the phosphorylations of IκB kinase (IKK)α/β, IκBα, and nuclear factor (NF)-κB-p65 proteins in human synoviocytes in a time-dependent manner. Treatment with neutralizing antibody for RAGE statistically significantly decreased the AGEs-induced increase in COX-2, VEGF, PGE2, IL-6, and MMP13 and AGEs-activated NF-κB pathway activation. Taken together, these findings indicate that AGEs are capable of inducing VEGF production and inflammatory responses via RAGE-NF-κB pathway activation in human synoviocytes. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:791-800, 2016.en_US
dc.language.isoenen_US
dc.publisherWILEYen_US
dc.relation.ispartofJournal of orthopaedic research : official publication of the Orthopaedic Research Societyen_US
dc.subjectadvanced glycation end products (AGEs); osteoarthritis; receptor for AGEs (RAGE); synoviocytes; vascular endothelial growth factoren_US
dc.subjectadvanced glycation end products (AGEs); osteoarthritis; receptor for AGEs (RAGE); synoviocytes; vascular endothelial growth factor-
dc.subject.otheradvanced glycation end product; advanced glycation end product receptor; cyclooxygenase 2; I kappa B kinase alpha; I kappa B kinase beta; immunoglobulin enhancer binding protein; interleukin 6; metalloproteinase; prostaglandin E2; transcription factor RelA; vasculotropin; advanced glycation end product; advanced glycation end product receptor; collagenase 3; cyclooxygenase 2; I kappa B; IL6 protein, human; immunoglobulin enhancer binding protein; interleukin 6; MMP13 protein, human; prostaglandin E2; PTGS2 protein, human; vasculotropin A; VEGFA protein, human; angiogenesis; Article; disease severity; enzyme phosphorylation; inflammation; priority journal; protein expression; signal transduction; synoviocyte; cell culture; human; inflammation; metabolism; synoviocyte; Cells, Cultured; Cyclooxygenase 2; Dinoprostone; Glycation End Products, Advanced; Humans; I-kappa B Proteins; Inflammation; Interleukin-6; Matrix Metalloproteinase 13; NF-kappa B; Receptor for Advanced Glycation End Products; Signal Transduction; Synoviocytes; Vascular Endothelial Growth Factor A-
dc.subject.other[SDGs]SDG3-
dc.titleAdvanced glycation end-products induced VEGF production and inflammatory responses in human synoviocytes via RAGE-NF-κB pathway activationen_US
dc.typejournal articleen_US
dc.identifier.doi10.1002/jor.23083-
dc.identifier.pmid26497299-
dc.identifier.scopus2-s2.0-84948799299-
dc.identifier.isiWOS:000375602200008-
dc.identifier.urlhttps://scholars.lib.ntu.edu.tw/handle/123456789/522973-
dc.relation.pages791en_US
dc.relation.journalvolume34en_US
dc.relation.journalissue5en_US
dc.relation.pageend800en_US
item.fulltextno fulltext-
item.languageiso639-1en-
item.openairetypejournal article-
item.openairecristypehttp://purl.org/coar/resource_type/c_6501-
item.cerifentitytypePublications-
item.grantfulltextnone-
crisitem.author.deptInternal Medicine-
crisitem.author.deptGeriatrics and Gerontology-NTUH-
crisitem.author.deptToxicology-
crisitem.author.deptIntegrated Diagnostics and Therapeutics-NTUH-
crisitem.author.deptInternal Medicine-
crisitem.author.deptInternal Medicine-NTUH-
crisitem.author.deptInstitute of Food Safety and Health-
crisitem.author.deptCenter for Biotechnology-
crisitem.author.deptPediatrics-
crisitem.author.deptPediatrics-NTUH-
crisitem.author.deptTraumatology-NTUH-
crisitem.author.deptSurgery-NTUHHC-
crisitem.author.deptLaboratory Medicine-
crisitem.author.deptLaboratory Medicine-NTUH-
crisitem.author.deptOrthopedic Surgery-NTUH-
crisitem.author.deptOrthopedic Surgery-
crisitem.author.orcid0000-0003-2215-2243-
crisitem.author.orcid0000-0001-9021-4616-
crisitem.author.orcid0000-0002-5954-5684-
crisitem.author.orcid0000-0001-8528-1566-
crisitem.author.orcid0000-0002-0553-4779-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgCollege of Public Health-
crisitem.author.parentorgOthers: University-Level Research Centers-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgNTU Hsin-Chu Hospital-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgCollege of Medicine-
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臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of “NTU Repository” with “Academic Hub” to form NTU Scholars.

總館學科館員 (Main Library)
醫學圖書館學科館員 (Medical Library)
社會科學院辜振甫紀念圖書館學科館員 (Social Sciences Library)

開放取用是從使用者角度提升資訊取用性的社會運動,應用在學術研究上是透過將研究著作公開供使用者自由取閱,以促進學術傳播及因應期刊訂購費用逐年攀升。同時可加速研究發展、提升研究影響力,NTU Scholars即為本校的開放取用典藏(OA Archive)平台。(點選深入了解OA)

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