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Reduction of platelet surface GPIb expression induced by polymorphonuclear leukocytes
M Schattner1, A Kempfer, J Geffner
1Departamento de Trombosis y Hemostasia, Instituto de Investigaciones Hematologicas, Academia Nacional de Medicina, Buenos Aires, Argentina.
Abstract:
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.
Insights
Polymorphonuclear neutrophils (PMNs) can inhibit platelet aggregation through a non-nitric oxide (NO) dependent mechanism. This study investigates how PMNs affect platelet surface receptors GPIb-IX and GPIIb-IIIa, impacting adhesion and aggregation.
Area of Science:
- Hematology
- Immunology
- Cellular Biology
Background:
- Soluble factors from polymorphonuclear neutrophils (PMNs) can activate platelets.
- PMNs may also inhibit platelet function, potentially via nitric oxide (NO) release.
- Previous observations indicate PMNs inhibit platelet aggregation and ATP release via a non-NO mechanism.
Purpose of the Study:
- To investigate the mechanism by which unstimulated PMNs inhibit platelet function.
- To evaluate the effect of PMNs on the expression of platelet glycoproteins GPIb-IX and GPIIb-IIIa.
Main Methods:
- Coincubation of platelets with unstimulated PMNs.
- Assessment of platelet aggregation and adenosine triphosphate (ATP) release.
- Evaluation of the expression of platelet glycoproteins GPIb-IX and GPIIb-IIIa.
Main Results:
- Unstimulated PMNs inhibit platelet aggregation and ATP release.
- The inhibitory mechanism does not involve nitric oxide (NO).
- PMNs modulate the expression of platelet surface receptors GPIb-IX and GPIIb-IIIa.
Conclusions:
- PMNs influence platelet function through a novel, non-NO dependent pathway.
- Alterations in platelet glycoprotein expression by PMNs may underlie inhibited platelet responses.
- Further research is needed to fully elucidate the non-identified mechanism.