The Effects of Anticoagulants on Cholangiocarcinoma Cell Induced Platelet Aggregation: a Comparison Between Sodium Citrate and Heparin

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Tipsuchon Aiamsa-ard
Pravit Akarasereenont
Sirikul Chotewuttakorn
Athiwat Thaworn

Abstract

During the transport of tumor cells in the blood, a variety of interactions can

occur  with host blood cells. Many studies showed that platelet activation by tumor

cells could lead to the formation of tumor microthrombi. However, different results

have been reported. Here, we examined whether anticoagulants, sodium citrate and

heparin, using in platelet rich plasma (PRP) preparation affected platelet aggregation

induced by Human Cholangiocarcinoma (HuCCA). Platelet aggregation was

measured by aggregometer. PRP was prepared from either sodium citrated- or

heparinized- blood. Primary HuCCA cells were cultured in our laboratory. Cells were

cultured in T-75 Flasks with Dulbeco Modified Eargle's Medium (DMEM)

containing 15 % fetal bovine serum, 100 units/ml penicillin G and 100 μg/ml

streptomycin. Cells were grown to confluence until uses, after which cells were

detached and, then, resuspended in DMEM to yield a concentration of 1x107 cells/ml.

150 μl of cell suspension or DMEM (control), therefore, were added to 850 μl of

either sodium citrated PRP (sPRP) or heparinized PRP (hPRP). To study cellular

mechanisms by which HuCCA induced platelet aggregation, signaling agents such as

apyrase, indomethacin, EDT A and hirudin will be used. HuCCA is able to induced

platelet aggregation in a direct tumor cell-platelet contacts. Interestingly, HuCCA

induced platelet aggregation was different in sPRP and hPRP. HuCCA could induce

platelet aggregation in some subjects of sPRP whereas induced in all subjects of

hPRP. Moreover, EDTA and indomethacin inhibited platelet aggregation induced by

HuCCA in both sPRP and hPRP. Hirudin inhibited platelet aggregation induced by

HuCCA in hPRP but not in sPRP whereas apyrase inhibited platelet aggregation

induced by HuCCA in sPRP but not in hPRP. Thus, this finding suggested that

anticoagulants used for platelet function studies could affect on signaling mechanism

of tumor cells induced platelet aggregation (TCIPA).

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Section
2002 Annual Meeting Abstracts/Lectures

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