Background: Platelet activation is critical during inflammation, thrombosis, and tumor progression and metastasis. This activation leads to platelet-monocyte aggregation, platelet P-selectin, and CD40 ligand (CD40L) expression. Platelets can increase acute myelogenous leukemia (AML) blast proliferation. Cilostazol is widely used for arteriosclerosis obliterans and is known to inhibit platelet function. We hypothesized that cilostazol preconditioning impairs subsequent AML blast proliferation through a reduction in platelet activation. We aim to determine the effects of cilostazol on platelet activation as measured by platelet-monocyte aggregation, platelet P-selectin, and CD40L expression. Methods: Platelet-rich plasma samples from healthy volunteers were treated with cilostazol. THP1 is a human AML cell line that resembles human monocytes, which was used as a model to measure platelet-monocyte aggregation. The blood samples were stimulated by adenosine diphosphate (8 μ M) for evaluation of platelet-monocytic THP1 cell aggregation and P-selectin expression and were stimulated by thrombin (0. 1 U/mL) for detecting CD40L expression. All samples were stained with fluorochrome-conjugated antibodies and were analyzed by flow cytometry. Results: Pretreatment with cilostazol significantly suppressed platelet-monocytic THP1 cell aggregation, P-selectin, and CD40L expression in a concentration-dependent manner at concentrations of 101, 102, and 103 mM, respectively. Conclusions: Our data showed that cilostazol can downregulate not only cellular interactions between platelets and monocytic THP1 cells but also platelet P-selectin and CD40L expression.
|Number of pages||7|
|Journal||Journal of Medical Sciences (Taiwan)|
|Publication status||Published - Feb 2009|
- THP1 cell
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