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学科主题: 临床医学
题名:
High Concentrations of Uric Acid Inhibit Endothelial Cell Migration via miR-663 Which Regulates Phosphatase and Tensin Homolog by Targeting Transforming Growth Factor-beta 1
作者: Hong, Quan1; Yu, Shandong2; Geng, Xiaodong1; Duan, Liping3; Zheng, Wei1; Fan, Men1; Chen, Xiangmei1; Wu, Di1
关键词: uric acid ; microRNA-663 ; transforming growth factor-1 ; phosphatase and tensin homolog ; endothelial cell migration
刊名: MICROCIRCULATION
发表日期: 2015-05-01
DOI: 10.1111/micc.12200
卷: 22, 期:4, 页:306-314
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Hematology ; Peripheral Vascular Disease
研究领域[WOS]: Hematology ; Cardiovascular System & Cardiology
关键词[WOS]: GROWTH-FACTOR ; PROMOTES ANGIOGENESIS ; RENAL-DISEASE ; DYSFUNCTION ; HYPERURICEMIA ; HYPERTENSION ; EXPRESSION ; PTEN ; MICRORNAS ; RISK
英文摘要:

BackgroundWhether microRNAs participate in endothelial dysfunction HUA remains unknown. A previous study indicated that miR-663 was the most significantly differentially expressed endothelial microRNA under HUA conditions. Some studies have demonstrated that the miR-663 target gene and TGF-1, promoted endothelial cell migration by inhibiting PTEN deleted on chromosome 10. Therefore, we hypothesized that HUA inhibits endothelial migration via miR-663, which regulates PTEN by targeting TGF-1.

MethodsPCR analysis was performed to determine miR-663 expression levels. A luciferase assay was performed to validate whether miR-663 targets TGF-1 directly. Western blot analysis was performed to determine TGF-1 and PTEN expression levels. An miR-663 inhibitor and TGF-1- and PTEN-specific siRNAs were transfected into EA.hy926 cells to inhibit miR-663, TGF-1, and PTEN expression, respectively. A wound healing assay was performed to determine the migratory ability of EA.hy926 cells.

ResultsmiR-663 had higher expression levels in HUA-stimulated endothelial cells and in the sera of hyperuricemic patients and animals. TGF-1 was targeted directly by miR-663. Endothelial miR-663 was up-regulated under HUA conditions, and HUA inhibited endothelial cell migration via miR-663, which targeted TGF-1. Thus, TGF-1 regulated cell migration in a PTEN-dependent manner.

ConclusionHUA inhibits endothelial cell migration via miR-663, which regulates PTEN by targeting TGF-1.

语种: 英语
所属项目编号: 31170810 ; 81470949 ; 61101218 ; Z121107002512078 ; 2012AA02A512 ; 2013CB530800 ; 2011BAI10B00
项目资助者: Chinese National Natural Sciences Foundation ; Beijing NOVA Program ; National High Technology Research and Development Program of China ; Major State Basic Research Development Program ; National Key Technology RD Program
WOS记录号: WOS:000353963800008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66391
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

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作者单位: 1.Chinese Peoples Liberat Army Gen Hosp, Chinese PLA Inst Nephrol, Natl Clin Res Ctr Kidney Dis, State Key Lab Kidney Dis,Dept Nephrol, Beijing 100853, Peoples R China
2.Peking Univ, Dept Cardiol, Hosp 1, Beijing 100871, Peoples R China
3.Chinese Peoples Liberat Army Gen Hosp, Registrat Dept, Beijing 100853, Peoples R China

Recommended Citation:
Hong, Quan,Yu, Shandong,Geng, Xiaodong,et al. High Concentrations of Uric Acid Inhibit Endothelial Cell Migration via miR-663 Which Regulates Phosphatase and Tensin Homolog by Targeting Transforming Growth Factor-beta 1[J]. MICROCIRCULATION,2015,22(4):306-314.
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