Epigallocatechin-3-O-Gallate, a Green Tea Polyphenol, Induces Expression of Pim-1 Kinase Via PPARγ in Human Vascular Endothelial Cells
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- 作者：Yan Liu (1)
Beilei Zhao (1)
Guangmei Mao (1)
Xi Fang (1)
Yahan Liu (1)
Yu Huang (3)
Nanping Wang (1) (2) - 关键词：Peroxisome proliferators ; activated receptors ; Pim ; 1 ; Endothelial cells ; Epigallocatechin ; 3 ; O ; gallate ; Green tea
- 刊名：Cardiovascular Toxicology
- 出版年：2013
- 出版时间：December 2013
- 年：2013
- 卷：13
- 期：4
- 页码：391-395
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- 作者单位：Yan Liu (1)
Beilei Zhao (1)
Guangmei Mao (1)
Xi Fang (1)
Yahan Liu (1)
Yu Huang (3)
Nanping Wang (1) (2)
1. Institute of Cardiovascular Science, Peking University Health Science Center, 38 Xueyuan Rd., Beijing, 100191, China
3. Institute of Vascular Medicine, Li Ka Shing Institute of Health Sciences, School of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong SAR, China
2. Cardiovascular Research Center, Xi’an Jiaotong University, Xi’an, 710061, China - ISSN：1559-0259
文摘
Pim-1 is a serine/threonine kinase and involved in cell survival and proliferation. Recently, it has been shown that pim-1 signaling pathway plays an important role in cardiovascular protection and differentiation. In this study, we sought to explore the expression of pim-1 in human vascular endothelial cells (ECs) and its regulation by epigallocatechin-3-O-gallate (EGCG), a green tea polyphenol which has anti-oxidant, anti-inflammatory and vascular protective effects. By using quantitative reverse transcriptase PCR (qRT-PCR) and Western blotting, we showed that EGCG dose-dependently increased the expression of pim-1 in cultured umbilical vein endothelial cells. Next, we showed that EGCG activated a luciferase reporter driven by peroxisome proliferators-activated receptor (PPAR)-responsive elements. The induced expression of pim-1 was inhibited in ECs pretreated with GW9662, a specific antagonist of PPARγ. In addition, pim-1 was also up-regulated in endothelial cells treated with rosiglitazone, a specific agonist for PPARγ, or those infected with the adenovirus expressing a constitutively active PPARγ. Collectively, our results provided new evidence that pim-1 can be up-regulated by EGCG via a PPARγ-mediated mechanism and may mediate its vascular protective effects.