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IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
Transcription factor Ap-1 mediates proangiogenic MIF expression in human endothelial cells exposed to Angiotensin II
作者: Shan, Zhi-Xin1,3; Lin, Qiu-Xiong1; Yang, Min1; Zhang, Bin1; Zhu, Jie-Ning1; Mai, Li-Ping1; Deng, Chun-Yu1; Liu, Ju-Li1; Zhang, You-Yi2; Lin, Shu-Guang1; Yu, Xi-Yong1
关键词: Angiotensin II ; Macrophage migration inhibitory factor ; AP-1 ; Endothelial cells ; Angiogenesis
刊名: CYTOKINE
发表日期: 2011
DOI: 10.1016/j.cyto.2010.09.009
卷: 53, 期:1, 页:35-41
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Cell Biology ; Immunology
研究领域[WOS]: Biochemistry & Molecular Biology ; Cell Biology ; Immunology
关键词[WOS]: MIGRATION-INHIBITORY FACTOR ; ACTIVATED PROTEIN-KINASE ; E-DEFICIENT MICE ; ATHEROSCLEROTIC PLAQUES ; SIGNAL-TRANSDUCTION ; PATHWAYS ; ANGIOGENESIS ; INSTABILITY ; BLOCKADE ; RECEPTOR
英文摘要:

Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine associated with the atherosclerotic process and atherosclerotic plaque stability. MIF was shown to be highly expressed in advanced atherosclerotic lesions. Neutralizing MIF with a blocking antibody induced a regression of established atherosclerotic lesions.

In this study, we investigated the mechanism underlying the proangiogenic effect of MIF in human umbilical vein endothelial cells (HUVECs). We showed that MIF induced the expression of angiogenesis-related genes in HUVECs. We also showed that MIF induced tube formation of HUVECs in vitro and in vivo. Angiotensin II (Ang II) could specifically up-regulate MIF expression in HUVECs. Using a luciferase reporter assay, we demonstrated that the AP-1 response element in the 5′-UTR of the MIF gene played a role in Ang II-induced MIF expression. Small hairpin RNA (shRNA) targeting c-Jun, a component of AP-1, and the AP-1 inhibitor CHX both efficiently inhibited MIF expression. The consistent result of electrophoretic mobility shift assay (EMSA) showed that Ang II specifically increased AP-1 activation in HUVECs. Our results suggest that AP-1 mediates Ang II-induced MIF expression which contributes to atherosclerotic plaque destabilization in human endothelial cells. (C) 2010 Elsevier Ltd. All rights reserved.

语种: 英语
所属项目编号: 30300421 ; 30672077 ; 30772142 ; 81070103 ; 2006CB503806
项目资助者: National Natural Science Foundation of China ; National Key Basic Research Program (NKBRP) of China
WOS记录号: WOS:000286862700008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57319
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Guangdong Acad Med Sci, Guangdong Gen Hosp, Res Ctr, Guangdong Prov Cardiovasc Inst, Guangzhou 510080, Guangdong, Peoples R China
2.Peking Univ Third Hosp, Inst Vasc Med, Beijing 100083, Peoples R China
3.Shantou Univ Med Coll, Dept Pharmacol, Shantou 515041, Peoples R China

Recommended Citation:
Shan, Zhi-Xin,Lin, Qiu-Xiong,Yang, Min,et al. Transcription factor Ap-1 mediates proangiogenic MIF expression in human endothelial cells exposed to Angiotensin II[J]. CYTOKINE,2011,53(1):35-41.
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