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Cordycepin inhibits vascular smooth muscle cell proliferation.

Authors
 Woochul Chang  ;  Soyeon Lim  ;  Heesang Song  ;  Byeong-Wook Song  ;  Hye-Jung Kim  ;  Min-Ji Cha  ;  Jae Mo Sung  ;  Tae Woong Kim  ;  Ki-Chul Hwang 
Citation
 EUROPEAN JOURNAL OF PHARMACOLOGY, Vol.597(1-3) : 64-69, 2008 
Journal Title
 EUROPEAN JOURNAL OF PHARMACOLOGY 
ISSN
 0014-2999 
Issue Date
2008
MeSH
Animals ; Basigin/metabolism ; Cardiovascular Agents/pharmacology* ; Carotid Artery Injuries/drug therapy* ; Carotid Artery Injuries/enzymology ; Carotid Artery Injuries/etiology ; Carotid Artery Injuries/pathology ; Catheterization/adverse effects ; Cell Movement/drug effects ; Cell Proliferation/drug effects* ; Cells, Cultured ; Collagen Type I/metabolism ; Cyclooxygenase 2/metabolism ; Deoxyadenosines/pharmacology* ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelial Cells/pathology ; Humans ; Male ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Muscle, Smooth, Vascular/drug effects* ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/injuries ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/drug effects* ; Myocytes, Smooth Muscle/enzymology ; Myocytes, Smooth Muscle/pathology ; Rats ; Rats, Sprague-Dawley
Keywords
Cordycepin ; Smooth muscle cell ; Restenosis ; Extracellular matrix ; Matrix metalloproteinase system
Abstract
Percutaneous transluminal coronary angioplasty (PTCA) is a common procedure for treating atherosclerosis, but its efficacy is limited because of the occurrence of restenosis within 3-6 months after angioplasty. Restenosis is induced by the remodeling of the vessel wall and/or the accumulation of cells and extracellular matrix (ECM) in the intimal layer. Therefore, the matrix metalloproteinase (MMP) system may be a potential therapeutic target for the treatment of restenosis or atherosclerosis. Cordycepin is reported to possess many pharmacological activities including immunological stimulating, anti-cancer, antioxidant, and anti-inflammatory activities. The effect of cordycepin on restenosis has not yet been clearly elucidated. Therefore, in the present study, we tested the role of cordycepin on the MMP system in vascular smooth muscle cells. In the carotid artery of a balloon-injured Sprague-Dawley (SD) rat, neointimal formation was reduced by treatment with cordycepin (20 microM/day, i.p), which inhibited the proliferation of rat aortic smooth muscle cells (RaoSMCs). To investigate the mechanism by which cordycepin inhibits the remodeling of the vessel wall and/or the accumulation of cells and ECM, we examined the activation of MMP systems in collagen type I-activated RaoSMCs. Cordycepin markedly inhibited the activation of MMP-2 and -9 as well as the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in a dose-dependent manner in collagen type I-activated RaoSMCs. Moreover, cordycepin suppressed cycloxygenase-2 (COX-2) expression related to hyperplasia of RAoSMCs. Taken together, these data suggest that cordycepin may induce antiproliferation in RAoSMCs via the modulation of vessel wall remodeling. Therefore, cordycepin may be a potential therapeutic approach to treat restenosis
Full Text
http://www.sciencedirect.com/science/article/pii/S0014299908008881
DOI
10.1016/j.ejphar.2008.08.030
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111148
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