Schattner M, Kempfer A, Geffner J, Bermejo E, Frontroth J P, Lazzari M
Departamento de Trombosis y Hemostasia, Instituto de Investigaciones Hematologicas, Academia Nacional de Medicina, Buenos Aires, Argentina.
Thromb Res. 1995 Aug 1;79(3):319-24. doi: 10.1016/0049-3848(95)00118-b.
It has been demonstrated that soluble factors released from PMNs such as proteases, free radicals and arachidonic acid metabolites are able to induce platelet activation (1). More recently, it has been demonstrated that PMNs can also inhibit platelet functional responses. It has been suggested that the inhibitory effect of PMNs could be related to the release of nitric oxide (NO) (2-3). In contrast, we have previously observed that coincubation of platelets with unstimulated PMNs, results in the inhibition of platelet aggregation and ATP release by a yet non-identified mechanism that does not involves NO (4). Considering that an alteration in surface receptors could be one of the phenomena accounting for impaired platelet responses, in the present study we evaluated the ability of PMNs to modulate the expression of the glycoproteins (GP) involved in platelet adhesion and aggregation, GPIb-IX and GPIIb-IIIa.
