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Human leukemia cells and mature lymphocytes induce platelet aggregation after removal of cell surface sialic acid
We examined platelet aggregating activity (PAA) of 5 human leukemia cell lines (HL-60, ML-1, HPB-ALL, RPMI-1788, K562), human mature lymphocytes and 2 human neuroblastoma lines (NCG, GOTO). Although intact cell suspensions of all leukemia cells and mature lymphocytes did not induce platelet aggregation, all cells exhibited PAA in both heparinized and citrated platelet rich plasma (PRP) following neuraminidase treatment (2 units/ml). In contrast, NCG and GOTO cells with PAA in intact cell suspensions were not affected by neuraminidase. PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment. Neuraminidase treatment had no effect on procoagulant activity of any of the cells examined. There was no difference in total sialic acid contents between human leukemia and neuroblastoma cells. These results suggest the cell surface glycoconjugates on hematopoietic cells play a role in PAA, and that sialic acid prevents their interaction with platelets.
We examined platelet aggregating activity (PAA) of 5 human leukemia cell lines (HL-60, ML-1, HPB-ALL, RPMI-1788, K562), human mature lymphocytes and 2 human neuroblastoma lines (NCG, GOTO). Although intact cell suspensions of all leukemia cells and mature lymphocytes did not induce platelet aggregation, all cells exhibited PAA in both heparinized and citrated platelet rich plasma (PRP) following neuraminidase treatment (2 units/ml). In contrast, NCG and GOTO cells with PAA in intact cell suspensions were not affected by neuraminidase. PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment. Neuraminidase treatment had no effect on procoagulant activity of any of the cells examined. There was no difference in total sialic acid contents between human leukemia and neuroblastoma cells. These results suggest the cell surface glycoconjugates on hematopoietic cells play a role in PAA, and that sialic acid prevents their interaction with platelets.