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. 2021 Jun;44(6):378-384.
doi: 10.1177/0391398820968849. Epub 2020 Nov 3.

Desialylation of platelet surface glycans enhances platelet adhesion to adsorbent polymers for lipoprotein apheresis

Lucia Lauková  1 , René Weiss  2 , Vladislav Semak  1 , Viktoria Weber  2
Affiliations

Desialylation of platelet surface glycans enhances platelet adhesion to adsorbent polymers for lipoprotein apheresis

Lucia Lauková et al. Int J Artif Organs. 2021 Jun.

Abstract

Background: Lipoprotein apheresis is an important therapeutic option in homozygous familial hypercholesterolemia, progressive atherosclerosis, or when depletion of lipoprotein(a) is indicated. It is generally regarded as safe, but drops in platelet counts as well as sporadic episodes of thrombocytopenia have been reported. We assessed the influence of platelet desialylation, which may be induced by endogenous or pathogen-derived neuraminidases, on platelet adhesion to polyacrylate-based adsorbents for whole blood lipoprotein apheresis.

Methods: Medical grade platelet concentrates were incubated with neuraminidase in vitro and were circulated over adsorbent columns downscaled from clinical application.

Results: Cleavage of terminal sialic residues resulted in platelet activation with significantly elevated expression of platelet factor 4 (PF4) and in enhanced platelet adhesion to the adsorbent, accompanied by a pronounced drop in platelet counts in the column flow-through.

Conclusion: Alterations in endogenous neuraminidase activity or exogenous (pathogen-derived) neuraminidase may trigger enhanced platelet adhesion in whole blood lipoprotein apheresis.

Keywords: Platelets; adsorption; glycosylation; sialylation.

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Conflict of interest statement

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Desialylation of platelet glycoproteins. Platelets were incubated with neuraminidase as described in the Methods section to cleave terminal sialic acid residues. Exposure of sialic acid and galactose residues was analyzed by flow cytometry after staining with Maackia amurensis lectin (MALII; panels a and c) and Ricinus Communis agglutinin (RCA; panels b and d).*p < 0.05; **p < 0.01; ***p < 0.001; n = 3.
Figure 2.
Figure 2.
Recirculation of platelet concentrates over adsorbent columns. Platelets were treated with neuraminidase (filled bars) or were left untreated (open bars) and were recirculated over columns containing polyacrylate-based DALI beads as described in the Methods section (panel a). Platelet counts in the pool were quanitified by cell counting (panel b), and the percentage of activated platelets was assessed by flow cytometry using P-selectin (CD62p) and platelet factor 4 (PF4) surface expression as indicator for platelet activation (panels c-d). *p < 0.05; **p < 0.01; ***p < 0.001; n = 4.
Figure 3.
Figure 3.
Scanning electron micrographs of adsorbent beads. Platelet concentrates without (panel a) and with (panel b) neuraminidase treatment were recirculated over DALI adsorbent columns as described in the Methods section. Thereafter, the columns were washed, fixed with glutaraldehyde, and analyzed using scanning electron microscopy.
See this image and copyright information in PMC

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