| Abstract |
Objective: To investigate whether cholangiocarcinoma (CCA) cells affected
platelet aggregation via activation of thrombin and cyclooxygenase.
Methods: Human cholangiocarcinoma (HuCCA) cells were cultured in T-75
Flasks with a standard technique. Cells were grown to confluence until
used, after which, cells were detached and then resuspended in DMEM.
Resuspended HuCCA cells were assessed for their effects on inducing
platelet aggregation of normal volunteers using Born's technique. Hirudin,
apyrase, EDTA and indomethacin were used as pharmacological tools to
investigate signaling mechanisms.
Results: HuCCA cells can initiate aggregation of platelets in heparinized
platelet rich plasma (hPRP). The potency of HuCCA cell induced platelet
aggregation depends on the concentration of cell suspension.
Interestingly, HuCCA cell induced platelet aggregation was inhibited by
hirudin (10, 20 and 40 unit), EDTA (2, 3 and 4 mM) and indomethacin (0.1,
1 and 2 mM) in a dose dependent manner but not by apyrase (5, 10 and 20
units).
Conclusion: HuCCA cells can induce platelet aggregation possibly via
activation of thrombin and the cyclooxygenase signaling pathway but not
the ADP pathway. Calcium may be an important factor required for this
reaction.
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