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Cilostazol inhibits high glucose- and angiotensin II-induced type 1 plasminogen activator inhibitor expression in artery wall and neointimal region after vascular injury

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Author(s)
김미경김혜순허승호박근규김형태조원현
Alternative Author(s)
Kim, Mi KyungKim, Hye SoonHur, Seung HoPark, Keun GyuKim, Hyoung TaeCho, Won Hyun
Publication Year
2009
Abstract
Increased expression of plasminogen activator inhibitor-1 (PAI-1) in vascular tissues is a potential factor
linking diabetes to restenosis after percutaneous coronary intervention. Recent studies have shown
that cilostazol, a selective type 3 phosphodiesterase inhibitor, prevents neointimal hyperplasia and instent
thrombosis in patients with diabetes after coronary angioplasty and stent implantation. However,
the molecular mechanism of this drug has not been fully elucidated. We examined whether cilostazol
inhibits PAI-1 expression in vascular smooth muscle cells (VSMCs) and neointimal hyperplasia.We found
that cilostazol effectively inhibits angiotensin II-, high glucose- and TGF- -stimulated PAI-1 expression
in vivo and in vitro. Cilostazol attenuated PAI-1 expression in neointimal regions and inhibited neointimal
hyperplasia after balloon injury. Cilostazol inhibited PAI-1 expression by multiple mechanisms including
downregulation of TGF- , JNK and p38 signaling pathways. Cilostazol also inhibited transactivating activity
at the PAI-1 promoter by Smad3, leading to a suppression of PAI-1 gene transcription. Taken together
with its antiproliferative effect on VSMCs, this may explain how cilostazol exerts its antithrombogenic
effects after angioplasty and stent implantation.
Department
Dept. of Internal Medicine (내과학)
Dept. of Surgery (외과학)
Publisher
School of Medicine
Citation
Atherosclerosis, Vol.207(2) : 391-398, 2009
Type
Article
ISSN
0021-9150
DOI
10.1016/j.atherosclerosis.2009.06.016
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35135
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