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学科主题: 临床医学
题名:
Uric acid promotes chemokine and adhesion molecule production in vascular endothelium via nuclear factor-kappa B signaling
作者: Liang, W. Y.1; Zhu, X. Y.2; Zhang, J. W.1; Feng, X. R.1; Wang, Y. C.1; Liu, M. L.1
关键词: Uric acid ; Hyperuricemia ; Atherosclerosis ; Chemokines ; Adhesion molecules ; NF-kappa B
刊名: NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
发表日期: 2015-02-01
DOI: 10.1016/j.numecd.2014.08.006
卷: 25, 期:2, 页:187-194
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Endocrinology & Metabolism ; Nutrition & Dietetics
研究领域[WOS]: Cardiovascular System & Cardiology ; Endocrinology & Metabolism ; Nutrition & Dietetics
关键词[WOS]: CORONARY-ARTERY-DISEASE ; NITRIC-OXIDE PRODUCTION ; SMOOTH-MUSCLE-CELLS ; C-REACTIVE PROTEIN ; ATHEROSCLEROSIS ; HYPERURICEMIA ; PROLIFERATION ; ATHEROGENESIS ; ASSOCIATION ; COHORT
英文摘要:

Background and aims: Hyperuricemia is an important risk factor for atherosclerosis, yet the potential mechanisms are not well understood. Migration and adhesion of leukocytes to endothelial cells play key roles in initiation and development of atherosclerosis. We investigated monocyte-endothelial cell interactions and potential signaling pathways under uric acid (UA)-stimulated conditions.

Methods and results: Primary human umbilical vein endothelial cells (HUVECs) were cultured and exposed to different concentrations of UA for various periods. Experimental hyperuricemia rat models were established. Expression of chemoattractant protein-1 (MCP-1), interleukin 8 (IL8), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were evaluated. Monocyteeendothelial cell interactions were elucidated by chemotaxis and adhesion assays, and nuclear factor-kappa B (NF-kB) pathway was studied using fluorescent microscopy and electrophoretic mobility shift assay. Results showed that high concentration of UA stimulated generation of chemokines and adhesion molecules in ex vivo and in vivo experiments. Migration and adhesion of human monocytic leukemia cell line THP-1 cells to HUVECs were promoted and activated NF-kB was significantly increased. UA-induced responses were ameliorated by organic anion transporter inhibitor probenecid and NF-kB inhibitor BAY117082. It was also observed that human endothelial cells expressed urate transporter-1, which was not regulated by UA.

Conclusion: High concentration of UA exerts unfavorable effects directly on vascular endothelium via the NF-kB signaling pathway, the process of which requires intracellular uptake of UA. (C) 2014 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 81170251
项目资助者: National Natural Science Foundation of China, China
WOS记录号: WOS:000349402700009
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/53560
Appears in Collections:北京大学首钢医院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Hosp 5, Dept Geriatr, Beijing 100034, Peoples R China
2.Peking Univ, Shougang Hosp, Dept Cardiol, Beijing 100034, Peoples R China

Recommended Citation:
Liang, W. Y.,Zhu, X. Y.,Zhang, J. W.,et al. Uric acid promotes chemokine and adhesion molecule production in vascular endothelium via nuclear factor-kappa B signaling[J]. NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES,2015,25(2):187-194.
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