Shear Stress Promotes Remodeling of Platelet Glycosylation via Upregulation of Platelet Glycosidase Activity

This dataset contains data related to the manuscript titled "Shear Stress Promotes Remodeling of Platelet Glycosylation via Upregulation of Platelet Glycosidase Activity: One More Thing" published in the Thrombosis and Haemostasis Journal (Thromb Haemost 2025; 125(04): 317-336, DOI: 10.1055/a-2398-9532). It contains flow cytometry data (FCS-files) indicating platelet surface glycosylation, expression of glycoprotein receptors on platelets and platelet-derived microparticles, as well as glycosidase activity data (MS Excel files) in human platelets, blood plasma, and serum.
We tested the hypothesis that shear stress induces remodeling of platelet surface glycosylation via upregulation of glycosidase activity, thus facilitating platelet count decline and intense microvesiculation. Human gel-filtered platelets were exposed to continuous shear stress of increasing magnitude in vitro with or without neuraminidase. Platelets and platelet-derived microparticles (PDMPs) were quantified via flow cytometry using size standard fluorescent nanobeads. Platelet surface glycosylation and NEU1 expression were evaluated using lectin- or immunostaining and multicolor flow cytometry. Platelet neuraminidase, galactosidase, hexosaminidase, and mannosidase activities were quantified using 4-methylumbelliferone-based fluorogenic substrates.
We demonstrated that shear stress promotes selective remodeling of platelet glycosylation via downregulation of 2,6-sialylation, terminal galactose, and mannose, while 2,3-sialylation remained largely unchanged. Shear-mediated deglycosylation is partially attenuated by neuraminidase inhibitors, strongly suggesting the involvement of platelet neuraminidase in observed phenomena. Shear stress increased platelet NEU1 surface expression and potentiated generation of numerous NEU1+ PDMPs. Platelets exhibited high basal hexosaminidase and mannosidase activities; basal activities of platelet neuraminidase and galactosidase were rather low and were significantly upregulated by shear stress. Shear stress of increased magnitude and duration promoted an incremental decline of platelet count and immense microvesiculation, both being further exacerbated by neuraminidase and partially attenuated by neuraminidase inhibition.
In summary, our data indicate that shear stress accumulation, consistent with supraphysiologic conditions of device-supported circulation, promotes remodeling of platelet glycosylation via selective upregulation of platelet glycosidase activity. Shear-mediated platelet deglycosylation is associated with platelet count drop and increased microvesiculation, thus offering a direct link between deglycosylation and thrombocytopenia observed in device-supported patients. Based on our findings, we propose a panel of molecular markers to be used for the reliable detection of shear-mediated platelet deglycosylation in MCS.