Uric Acid Induces Endothelial Dysfunction by Activating the HMGB1/RAGE Signaling Pathway.
Uric acid (UA) is a risk factor for endothelial dysfunction, a process in which inflammation may play an important role. UA increases high mobility group box chromosomal protein 1 (HMGB1) expression and extracellular release in endothelial cells. HMGB1 is an inflammatory cytokine that interacts with...
| Publicado en: | BioMed Research International Vol. 2017; pp. 1 - 12 |
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| Autores principales: | , , , , , , , , , |
| Formato: | pictorial research tables/charts Journal Article |
| Publicado: |
Wiley-Blackwell
1/1/2017
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=120493687&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 120493687 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 23146133 FT2T jtl: BioMed Research International issn: 23146133 maglogo: N pubinfo: dt: 1/1/2017 vid: 2017 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 120493687 120493687 120493687 10.1155/2017/4391920 120493687 ppf: 1 ppct: 11 formats: fmt: @attributes: type: P tig: atl: Uric Acid Induces Endothelial Dysfunction by Activating the HMGB1/RAGE Signaling Pathway. aug: au: Cai, Wei Duan, Xi-Mei Liu, Ying Yu, Jiao Tang, Yun-Liang Liu, Ze-Lin Jiang, Shan Zhang, Chun-Ping Liu, Jian-Ying Xu, Ji-Xiong affil: Department of Endocrinology and Metabolism, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China sug: subj: Uric Acid Administration and Dosage Signal Transduction Endothelium Physiopathology Cytokines Receptors, Cell Surface Glycation End Products, Advanced Human Cell Culture Techniques Umbilical Veins Inflammation NF-kappa B Cell Adhesion Molecules Nitric Oxide Oxidoreductases RNA Analysis Polymerase Chain Reaction Methods Blotting, Western P-Value Enzyme-Linked Immunosorbent Assay T-Tests One-Way Analysis of Variance Post Hoc Analysis Data Analysis Software Descriptive Statistics Funding Source ab: Uric acid (UA) is a risk factor for endothelial dysfunction, a process in which inflammation may play an important role. UA increases high mobility group box chromosomal protein 1 (HMGB1) expression and extracellular release in endothelial cells. HMGB1 is an inflammatory cytokine that interacts with the receptor for advanced glycation end products (RAGE), inducing an oxidative stress and inflammatory response, which leads to endothelial dysfunction. In this study, human umbilical vein endothelial cells (HUVECs) were incubated with a high concentration of UA (20 mg/dL) after which endothelial function and the expression of HMGB1, RAGE, nuclear factor kappa B (NF-κB), inflammatory cytokines, and adhesion molecules were evaluated. UA inhibited endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production in HUVECs, increased intracellular HMGB1 expression and extracellular HMGB1 secretion, and upregulated RAGE expression. UA also activated NF-κB and increased the level of inflammatory cytokines. Blocking RAGE significantly suppressed the upregulation of RAGE and HMGB1 and prevented the increase in DNA binding activity of NF-κB and the levels of inflammatory cytokines. It also blocked the decrease in eNOS expression and NO production induced by UA. Our results suggest that high concentrations of UA cause endothelial dysfunction via the HMGB1/RAGE signaling pathway. pubtype: Academic Journal doctype: pictorial research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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