Membrane-Activated Form of Glycoproteins IIb/IIIa Complex on Newborn Platelets

Abstract

Background: GPIIb/IIIa complex is one of the laboratory markers of platelet activation. Closely associated with this process is exposure of the fibrinogen-binding site which is essential for platelets aggregation. This study was performed to evaluate the expression of GPIIb/IIIa on the platelets at time of birth. Materials and Methods: 51 term newborns, 21 females and 30 males, were introduced to the study. They fitted all criteria for healthy term newborns. Blood was collected from umbilical artery and vein immediately after cutting the umbilical cord using Diatube TM CTAD Vacutainer System. GPIIb/IIIa was tested with PAC-1-FITC antibody using flow cytometer EPICS XL. Results: 90.91% of newborn platelets express GPIIb/IIIa complex in comparison to adults, where only 12.79% platelets express this complex. Practically no differences were noted in relation to gender of newborns and umbilical artery or vein. Conclusions: Careful analysis of the presented data reveals that at time of birth platelets are hyperreactive, which may be related to the increased thrombogenesis in newborns and mothers.

Comparative evaluation of PAR1, GPIb-IX-V, and integrin αIIbβ3 levels in cord and adult platelets

“…Since the surface expression of integrin αIIbβ3 is a good marker for platelet activation, these variations are probably due to differences in sample acquisition and preparation. In one study lower surface levels of the marker have been found, while another study found significantly higher values arguing for thrombogenesis during birth (8,9). Poor response to epinephrin might be caused by lower levels of α 2 -adrenergetic receptors (10).…”

Ontogeny of platelet function

“…Therefore, the results should be interpreted with caution. 37 Of interest, Caparr ós-P érez et al performed a platelet transcriptome analysis and showed variations in the neonatal platelet transcriptome compared with adults. 38 In fact, they reported that genes involved in cell signaling and calcium metabolism were among those most downregulated in neonatal platelets.…”