Cilostazol Induces eNOS and TM Expression via Activation with Sirtuin 1/Krüppel-like Factor 2 Pathway in Endothelial Cells

Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilost...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-10, Vol.22 (19), p.10287
Main Authors: Wu, Chih-Hsien, Chiu, Yi-Lin, Hsieh, Chung-Yueh, Tsung, Guo-Shiang, Wu, Lian-Shan, Cheng, Cheng-Chung, Tsai, Tsung-Neng
Format: Article
Language:English
Subjects:
Arteriosclerosis
Atherosclerosis
Bioavailability
Blood clots
Blood platelets
Cardiovascular system
Cell adhesion & migration
Cell cycle
cilostazol
Drug dosages
Endothelial cells
endothelial nitric oxide synthase
Flow cytometry
Gene expression
Homeostasis
Implants
Kinases
Krueppel-like factor
Krüppel-like factor 2
Nitric oxide
Nitric-oxide synthase
Patients
Proteins
Shear stress
SIRT1 protein
Smooth muscle
Stents
thrombomodulin
Thrombosis
Transcription
Umbilical vein
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Summary:Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilostazol. Human umbilical vein endothelial cells (HUVECs) were cultured with various concentrations of cilostazol to verify its impact on endothelial cells. KLF2, silent information regulator transcript-1 (SIRT1), endothelial nitric oxide synthase (eNOS), and endothelial thrombomodulin (TM) expression levels were examined. We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion. The activation was regulated by SIRT1, which was also stimulated by cilostazol. These findings suggest that cilostazol may be capable of an antithrombotic and vasculoprotective effect in endothelial cells.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms221910287