Aggregation of human peripheral blood mononuclear cells by calcium ionophore A23187. Comparison with the aggregation of platelets and defective response in Glanzmann's thrombasthenia

Cerbone, A.M.; Di Minno, G.; Montemurro, P.; Iride, C.; Ciavarella, N.; Scillitani, A.; Semeraro, N.

Agents and Actions 24(1-2): 165-171

1988


ISSN/ISBN: 0065-4299
PMID: 3136623
DOI: 10.1007/bf01968096
Accession: 039206084

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Abstract
Following exposure to calcium ionophore A23187, washed peripheral blood mononuclear cells (MNC) aggregated and formed thromboxane, like platelets. However, while aspirin strongly inhibited platelet aggregation and thromboxane formation, it had a little effect on the aggregation of MNC. In about 50% of the samples studied, aggregation of MNC was associated with the secretion of ATP. However studies in which exogenous ATP or ADP were used, suggested that the aggregation of MNC is independent of the secretion of nucleotides. MNC from 2 thrombasthenic patients failed to aggregate and bound 9-10 fold less radiolabelled fibrinogen than those from normals when challenged with A23187. However, fibrinogen, which plays a major role in the aggregation of platelets, did not appear to be involved in the aggregation of MNC. A differing behavior of these two types of cells was also found when the effect of plasma was studied on the aggregation response to A23187. Indeed, citrated plasma greatly enhanced the aggregation of platelets while it suppressed the response to MNC. This inhibitory effect of plasma was not detected when heparinized plasma was substituted for citrated plasma. We conclude that the aggregation of MNC in response to A23187 does not involve basic events known to play a major role in the aggregation of platelets. The response to A23187 may be an important probe for understanding basic mechanisms and pathophysiological significance of the aggregation of MNC.

Aggregation of human peripheral blood mononuclear cells by calcium ionophore A23187. Comparison with the aggregation of platelets and defective response in Glanzmann's thrombasthenia