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Tytuł:
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Evaluation of the antiplatelet effects of cilostazol, a phosphodiesterase 3 inhibitor, by VASP phosphorylation and platelet aggregation.
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Autorzy:
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Yamamoto H; Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Honmachi, Sakyo-ku, Kyoto, Japan.
Takahashi K
Watanabe H
Yoshikawa Y
Shirakawa R
Higashi T
Kawato M
Ikeda T
Tabuchi A
Morimoto T
Kita T
Horiuchi H
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Źródło:
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Circulation journal : official journal of the Japanese Circulation Society [Circ J] 2008 Nov; Vol. 72 (11), pp. 1844-51. Date of Electronic Publication: 2008 Oct 03.
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Typ publikacji:
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Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Original Publication: Kyoto, Japan : Japanese Circulation Society, [2002-
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MeSH Terms:
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Phosphodiesterase 3 Inhibitors*
Blood Platelets/*metabolism
Cell Adhesion Molecules/*metabolism
Microfilament Proteins/*metabolism
Phosphoproteins/*metabolism
Platelet Aggregation/*drug effects
Platelet Aggregation Inhibitors/*administration & dosage
Tetrazoles/*administration & dosage
Adult ; Alprostadil/pharmacology ; Cilostazol ; Humans ; Male ; Middle Aged ; Phosphorylation/drug effects
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Substance Nomenclature:
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0 (Cell Adhesion Molecules)
0 (Microfilament Proteins)
0 (Phosphodiesterase 3 Inhibitors)
0 (Phosphoproteins)
0 (Platelet Aggregation Inhibitors)
0 (Tetrazoles)
0 (vasodilator-stimulated phosphoprotein)
F5TD010360 (Alprostadil)
N7Z035406B (Cilostazol)
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Entry Date(s):
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Date Created: 20081004 Date Completed: 20081230 Latest Revision: 20190819
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Update Code:
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20240104
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DOI:
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10.1253/circj.cj-08-0289
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PMID:
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18832777
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Background: Cilostazol, a phosphodiesterase 3 inhibitor, is an antiplatelet drug that is widely used for preventing cardiovascular events, although, to date, there are few methods for evaluating its effects.
Methods and Results: Blood samples were taken at baseline and at 3 and 12 h in 10 healthy male subjects after 100 mg cilostazol intake. Each sample was examined by Western blot for phosphorylation levels of vasodilator-stimulated phosphoprotein (VASP), an abundant cAMP-dependent kinase substrate in platelets, and by the optical aggregometer for ADP- and collagen-induced aggregation, before and after 8 nmol/L prostaglandin E(1) (PGE(1)) treatment. Cilostazol intake did not affect VASP phosphorylation levels or the maximal aggregation rates without PGE(1) treatment. However, cilostazol intake apparently enhanced PGE(1)-induced VASP phosphorylation and PGE(1)-mediated reduction of ADP-and collagen-induced maximal aggregation rates. Levels of VASP phosphorylated at Ser157 were correlated and the maximal aggregation rates induced by ADP were inversely correlated with cilostazol concentrations in the plasma.
Conclusion: The antiplatelet effects of cilostazol intake could be evaluated by measuring VASP phosphorylation levels and maximal aggregation rates in platelets by ex vivo treatment with a low concentration of PGE(1).