TY - JOUR
T1 - Epigallocatechin-3-o-gallate, a green tea polyphenol, induces expression of pim-1 kinase via PPARγ in human vascular endothelial cells
AU - Liu, Yan
AU - Zhao, Beilei
AU - Mao, Guangmei
AU - Fang, Xi
AU - Liu, Yahan
AU - Huang, Yu
AU - Wang, Nanping
PY - 2013/12
Y1 - 2013/12
N2 - 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.
AB - 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.
KW - Endothelial cells
KW - Epigallocatechin-3-O-gallate
KW - Green tea
KW - Peroxisome proliferators-activated receptors
KW - Pim-1
UR - https://www.scopus.com/pages/publications/84890571476
U2 - 10.1007/s12012-013-9220-4
DO - 10.1007/s12012-013-9220-4
M3 - 文章
C2 - 23990052
AN - SCOPUS:84890571476
SN - 1530-7905
VL - 13
SP - 391
EP - 395
JO - Cardiovascular Toxicology
JF - Cardiovascular Toxicology
IS - 4
ER -