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PPAR-alpha Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5 ′-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells
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
2011
DOI10.1155/2011/523520
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
WOS记录号WOS:000298691800001
项目编号2011CB503904 ; 30730042 ; 30770873 ; 81070244
资助机构Major National Basic Research Program of China ; Chinese National Natural Science Foundation
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56938
专题北京大学第三临床医学院_内分泌科
北京大学基础医学院
北京大学第三临床医学院_心血管内科
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
推荐引用方式
GB/T 7714
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.
APA Liu, Jinbo.,Lu, Changlin.,Li, Fuwang.,Wang, Haining.,He, Liyun.,...&Wang, Guang.(2011).PPAR-alpha Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5 ′-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells.PPAR RESEARCH.
MLA Liu, Jinbo,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".PPAR RESEARCH (2011).
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