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学科主题基础医学
Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation
Zhu, Zhenjiu1; Fu, Chenglai1; Li, Xiaoxia1; Song, Yimeng1; Li, Chenghong1; Zou, Minghui2; Guan, Youfei1; Zhu, Yi1
刊名PLOS ONE
2011-08-18
DOI10.1371/journal.pone.0023554
6期:8
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]ADIPONECTIN STIMULATES ANGIOGENESIS ; TRANSPLANTED HUMAN HEART ; PROTEIN-KINASE ; PROGENITOR CELLS ; CANCER CELLS ; CYCLOOXYGENASE-2 EXPRESSION ; MYOCARDIAL-INFARCTION ; COX-2 EXPRESSION ; RECEPTOR SUBTYPE ; IN-VIVO
英文摘要

Prostaglandin E2 (PGE2) has been reported to modulate angiogenesis, the process of new blood vessel formation, by promoting proliferation, migration and tube formation of endothelial cells. Endothelial progenitor cells are known as a subset of circulating bone marrow mononuclear cells that have the capacity to differentiate into endothelial cells. However, the mechanism underlying the stimulatory effects of PGE2 and its specific receptors on bone marrow-derived cells (BMCs) in angiogenesis has not been fully characterized. Treatment with PGE2 significantly increased the differentiation and migration of BMCs. Also, the markers of differentiation to endothelial cells, CD31 and von Willebrand factor, and the genes associated with migration, matrix metalloproteinases 2 and 9, were significantly upregulated. This upregulation was abolished by dominant-negative AMP-activated protein kinase (AMPK) and AMPK inhibitor but not protein kinase, a inhibitor. As a functional consequence of differentiation and migration, the tube formation of BMCs was reinforced. Along with altered BMCs functions, phosphorylation and activation of AMPK and endothelial nitric oxide synthase, the target of activated AMPK, were both increased which could be blocked by EP4 blocking peptide and simulated by the agonist of EP4 but not EP1, EP2 or EP3. The pro-angiogenic role of PGE2 could be repressed by EP4 blocking peptide and retarded in EP4(+/-) mice. Therefore, by promoting the differentiation and migration of BMCs, PGE2 reinforced their neovascularization by binding to the receptor of EP4 in an AMPK-dependent manner. PGE2 may have clinical value in ischemic heart disease.

语种英语
WOS记录号WOS:000294126900028
项目编号2010CB912504 ; 308201001 ; 810701113 ; 81028002
资助机构Major National Basic Research Grant of China ; National Natural Science Foundation of China ; "111" plan of China
引用统计
被引频次:24[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/400002259/67997
专题北京大学基础医学院_心血管所
北京大学基础医学院
北京大学第三临床医学院_泌尿外科
作者单位1.Peking Univ, Key Lab Mol Cardiovasc Sci, Educ Minist, Dept Physiol & Pathophysiol,Hlth Sci Ctr, Beijing 100871, Peoples R China
2.Univ Oklahoma, Hlth Sci Ctr, Dept Med, Div Endocrinol & Diabet, Oklahoma City, OK USA
推荐引用方式
GB/T 7714
Zhu, Zhenjiu,Fu, Chenglai,Li, Xiaoxia,et al. Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation[J]. PLOS ONE,2011,6(8).
APA Zhu, Zhenjiu.,Fu, Chenglai.,Li, Xiaoxia.,Song, Yimeng.,Li, Chenghong.,...&Zhu, Yi.(2011).Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation.PLOS ONE,6(8).
MLA Zhu, Zhenjiu,et al."Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation".PLOS ONE 6.8(2011).
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