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Tranilast inhibits the proliferation of human coronary smooth muscle cell through the activation of p21waf1

被引：36
作者：
Kusama, H
Kikuchi, S
Tazawa, S
Katsuno, K
Baba, Y
Zhai, YL
Nikaido, T
Fujii, S
机构：
[1] Kissei Pharmaceut Co Ltd, Discovery Res Labs, Nagano 3998304, Japan
[2] Shinshu Univ, Sch Med, Dept Obstet & Gynecol, Matsumoto, Nagano 3908621, Japan
[3] Kyoto Univ, Fac Med, Dept Obstet & Gynecol, Sakyo Ku, Kyoto 6068397, Japan
来源：
ATHEROSCLEROSIS | 1999年 / 143卷 / 02期
关键词：
CDK; p21(waf1); p53; proliferation; PTCA; smooth muscle cell; tranilast;
D O I：
10.1016/S0021-9150(98)00308-6
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Restenosis after percutaneous transluminal coronary angioplasty (PTCA) occurs due to vascular smooth muscle cell proliferation and migration. Recently, tranilast, an anti-allergic drug, has been used for the prevention of restenosis after PTCA. To determine the molecular mechanism involved, the effect of tranilast on the proliferation of human coronary smooth muscle cells (SMCs) was investigated. Tranilast arrested the proliferation of human coronary SMCs at the G0/G1 phase of the cell cycle. In association with this inhibitory effect, tranilast increased p21(waf1) and p53 tumor suppressor factor, and decreased cyclin-dependent kinase 2 (CDK2) activity. These results suggest that tranilast inhibits the proliferation of human coronary SMCs during restenosis after PTCA via an induction of p21(waf1) and p53. Tranilast may thus allow us to prevent restenosis after PTCA by interfering with this mechanism. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
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收藏
页码：307 / 313
页数：7
相关论文
共 18 条
[1]   PHARMACOLOGICAL PROPERTIES OF N-(3',4'-DIMETHOXYCINNAMOYL) ANTHRANILIC ACID (N-5'), A NEW ANTI-ATOPIC AGENT [J].
AZUMA, H ;
BANNO, K ;
YOSHIMURA, T .
BRITISH JOURNAL OF PHARMACOLOGY, 1976, 58 (04) :483-488
[2]   WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].
ELDEIRY, WS ;
TOKINO, T ;
VELCULESCU, VE ;
LEVY, DB ;
PARSONS, R ;
TRENT, JM ;
LIN, D ;
MERCER, WE ;
KINZLER, KW ;
VOGELSTEIN, B .
CELL, 1993, 75 (04) :817-825
[3]   Inhibition of smooth muscle cell migration by the p21 cyclin-dependent kinase inhibitor (Cip1) [J].
Fukui, R ;
Shibata, N ;
Kohbayashi, E ;
Amakawa, M ;
Furutama, D ;
Hoshiga, M ;
Negoro, N ;
Nakakouji, T ;
Ii, M ;
Ishihara, T ;
Ohsawa, N .
ATHEROSCLEROSIS, 1997, 132 (01) :53-59
[4]   Inhibitory effects of tranilast on proliferation, migration, and collagen synthesis of human vascular smooth muscle cells [J].
Fukuyama, J ;
Miyazawa, K ;
Hamano, S ;
Ujiie, A .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1996, 74 (01) :80-84
[5]   INTIMAL HYPERPLASIA, VASCULAR MODELING, AND THE RESTENOSIS PROBLEM [J].
GLAGOV, S .
CIRCULATION, 1994, 89 (06) :2888-2891
[6]  
HAN DKM, 1995, AM J PATHOL, V147, P267
[7]   SELECTIVE-INHIBITION OF COLLAGEN ACCUMULATION BY N-(3,4-DIMETHOXYCINNAMOYL)ANTHRANILIC ACID (N-5') IN GRANULATION-TISSUE [J].
ISAJI, M ;
NAKAJOH, M ;
NAITO, J .
BIOCHEMICAL PHARMACOLOGY, 1987, 36 (04) :469-474
[8]  
Kato K., 1996, RINSHO IYAKU, V12, P65
[9]   Tranilast suppresses intimal hyperplasia after photochemically induced endothelial injury in the rat [J].
Kikuchi, S ;
Umemura, K ;
Kondo, K ;
Nakashima, M .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1996, 295 (2-3) :221-227
[10]   Photochemically induced endothelial injury in the mouse as a screening model for inhibitors of vascular intimal thickening [J].
Kikuchi, S ;
Umemura, K ;
Kondo, K ;
Saniabadi, AR ;
Nakashima, M .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (07) :1069-1078
12