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学科主题: 临床医学
题名:
PPAR-alpha Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5 ′-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells
作者: Liu, Jinbo1; Lu, Changlin2; Li, Fuwang3,4; Wang, Haining1; He, Liyun5; Hao, Yanting5; Chen, Alex F.6; An, Huijie1; Wang, Xian3,4; Hong, Tianpei1; Wang, Guang1
刊名: PPAR RESEARCH
发表日期: 2011
DOI: 10.1155/2011/523520
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Medicine, Research & Experimental
研究领域[WOS]: Research & Experimental Medicine
关键词[WOS]: NITRIC-OXIDE SYNTHASE ; CORONARY-ARTERY-DISEASE ; DYSFUNCTION ; OVEREXPRESSION ; ATHEROSCLEROSIS ; PRESSURE ; STRESS ; GENE ; MICE
英文摘要:

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide (NO) synthase. Guanosine 5′-triphosphate cyclohydrolase-I (GTPCH-I) is a key limiting enzyme for BH4 synthesis. In the present in vitro study, we investigated whether peroxisome proliferator-activated receptor alpha (PPAR-alpha) agonist fenofibrate could recouple eNOS by reversing low-expression of intracellular BH4 in endothelial cells and discussed the potential mechanisms. After human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS) for 24 hours, the levels of cellular eNOS, BH4 and cell supernatant NO were significantly reduced compared to control group. And the fluorescence intensity of intracellular ROS was significantly increased. But pretreated with fenofibrate (10 umol/L) for 2 hours before cells were induced by LPS, the levels of eNOS, NO, and BH4 were significantly raised compared to LPS treatment alone. ROS production was markedly reduced in fenofibrate group than LPS group. In addition, our results showed that the level of intracellular GTPCH-I detected by western blot was increased in a concentration-dependent manner after being treated with fenofibrate. These results suggested that fenofibrate might help protect endothelial function and against atherosclerosis by increasing level of BH4 and decreasing production of ROS through upregulating the level of intracellular GTPCH-I.

语种: 英语
所属项目编号: 2011CB503904 ; 30730042 ; 30770873 ; 81070244
项目资助者: Major National Basic Research Program of China ; Chinese National Natural Science Foundation
WOS记录号: WOS:000298691800001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/56938
Appears in Collections:北京大学第三临床医学院_内分泌科_期刊论文

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作者单位: 1.Peking Univ Third Hosp, Dept Endocrinol, Beijing 100191, Peoples R China
2.Beijing Tongren Hosp, Dept Cardiol, Beijing 100191, Peoples R China
3.Peking Univ Hlth Sci Ctr, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
4.Peking Univ Hlth Sci Ctr, Key Lab Mol Cardiovasc Sci, Minist Educ, Beijing 100191, Peoples R China
5.Peking Univ Third Hosp, Dept Cardiovasc Med, Beijing 100191, Peoples R China
6.Univ Pittsburgh, Sch Med & Vasc Surg Res, Dept Surg, Pittsburgh, PA 15240 USA

Recommended Citation:
Liu, Jinbo,Lu, Changlin,Li, Fuwang,et al. PPAR-alpha Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5 ′-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells[J]. PPAR RESEARCH,2011.
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