Abstract
Daily green tea drinking showed preventive effects on the progression of atherosclerosis. Although epigallocatechin-3-gallate [EGCG] has anti-proliferative effects on various cells, relatively little is known about the molecular mechanisms of the anti-proliferative effects of EGCG. To determine whether the transduction signals and protooncogene expression were affected by EGCG, this study investigated the molecular mechanism of the anti-proliferative effects in basic fibroblast growth factor (bFGF)-stimulated rat aortic smooth muscle cells (RAoSMCs). EGCG inhibited the proliferative response stimulated by 10% fetal bovine serum dose dependently in RAoSMCs (median inhibitory concentration [IC50]: 28.4 × 10-6 M). EGCG also inhibited the migration of bFGF-stimulated RAoSMCs in a dose-dependent manner, showing that 21.8 × 10-6 M of EGCG significantly inhibited the migration by 75 ± 5% in comparison with bFGF-stimulated migration. In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression. Induction of c-jun mRNA stimulated by bFGF was significantly reduced dose dependently up to 87.3 × 10-6 M of EGCG. These results indicate that the anti-proliferative effect of EGCG on RAoSMCs is partly Ras/JNK mediated, independent of protein kinase C, and is attributable to the downregulation of c-jun expression.
| Original language | English |
|---|---|
| Pages (from-to) | 271-277 |
| Number of pages | 7 |
| Journal | Journal of Cardiovascular Pharmacology |
| Volume | 39 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2002 Feb 5 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
- Cardiology and Cardiovascular Medicine
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Epigallocatechin-3-gallate inhibits basic fibroblast growth factor-induced intracellular signaling transduction pathway in rat aortic smooth muscle cells. / Hwang, Ki Chul; Lee, Kyung Hye; Jang, Yangsoo; Yun, Yeo Pyo; Chung, Kwang Hoe.
In: Journal of Cardiovascular Pharmacology, Vol. 39, No. 2, 05.02.2002, p. 271-277.Research output: Contribution to journal › Article
TY - JOUR
T1 - Epigallocatechin-3-gallate inhibits basic fibroblast growth factor-induced intracellular signaling transduction pathway in rat aortic smooth muscle cells
AU - Hwang, Ki Chul
AU - Lee, Kyung Hye
AU - Jang, Yangsoo
AU - Yun, Yeo Pyo
AU - Chung, Kwang Hoe
PY - 2002/2/5
Y1 - 2002/2/5
N2 - Daily green tea drinking showed preventive effects on the progression of atherosclerosis. Although epigallocatechin-3-gallate [EGCG] has anti-proliferative effects on various cells, relatively little is known about the molecular mechanisms of the anti-proliferative effects of EGCG. To determine whether the transduction signals and protooncogene expression were affected by EGCG, this study investigated the molecular mechanism of the anti-proliferative effects in basic fibroblast growth factor (bFGF)-stimulated rat aortic smooth muscle cells (RAoSMCs). EGCG inhibited the proliferative response stimulated by 10% fetal bovine serum dose dependently in RAoSMCs (median inhibitory concentration [IC50]: 28.4 × 10-6 M). EGCG also inhibited the migration of bFGF-stimulated RAoSMCs in a dose-dependent manner, showing that 21.8 × 10-6 M of EGCG significantly inhibited the migration by 75 ± 5% in comparison with bFGF-stimulated migration. In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression. Induction of c-jun mRNA stimulated by bFGF was significantly reduced dose dependently up to 87.3 × 10-6 M of EGCG. These results indicate that the anti-proliferative effect of EGCG on RAoSMCs is partly Ras/JNK mediated, independent of protein kinase C, and is attributable to the downregulation of c-jun expression.
AB - Daily green tea drinking showed preventive effects on the progression of atherosclerosis. Although epigallocatechin-3-gallate [EGCG] has anti-proliferative effects on various cells, relatively little is known about the molecular mechanisms of the anti-proliferative effects of EGCG. To determine whether the transduction signals and protooncogene expression were affected by EGCG, this study investigated the molecular mechanism of the anti-proliferative effects in basic fibroblast growth factor (bFGF)-stimulated rat aortic smooth muscle cells (RAoSMCs). EGCG inhibited the proliferative response stimulated by 10% fetal bovine serum dose dependently in RAoSMCs (median inhibitory concentration [IC50]: 28.4 × 10-6 M). EGCG also inhibited the migration of bFGF-stimulated RAoSMCs in a dose-dependent manner, showing that 21.8 × 10-6 M of EGCG significantly inhibited the migration by 75 ± 5% in comparison with bFGF-stimulated migration. In RAoSMCs, EGCG dramatically inhibited Ras activation and c-jun N-terminal kinase (JNK) activity without affecting protein kinase C expression. Induction of c-jun mRNA stimulated by bFGF was significantly reduced dose dependently up to 87.3 × 10-6 M of EGCG. These results indicate that the anti-proliferative effect of EGCG on RAoSMCs is partly Ras/JNK mediated, independent of protein kinase C, and is attributable to the downregulation of c-jun expression.
UR - http://www.scopus.com/inward/record.url?scp=0036146830&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036146830&partnerID=8YFLogxK
U2 - 10.1097/00005344-200202000-00014
DO - 10.1097/00005344-200202000-00014
M3 - Article
C2 - 11791013
AN - SCOPUS:0036146830
VL - 39
SP - 271
EP - 277
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 2
ER -