MCS Hypershear Modulates Platelet Membrane Fluidity, Lipid Species, and is Gender Specific

Sweedo, Alice; Wise, Lisa M.; Sheriff, Jawaad; Bluestein, Danny; Purdy, John; Slepian, Marvin J.

doi:10.1016/j.healun.2020.01.1075

Cited by 3 publications

(1 citation statement)

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“…We have previously demonstrated that biomechanical properties of platelets including overall cell stiffness [33], regional membrane stiffness [34,35], and membrane fluidity [36,37] are major determinants of shear-mediated platelet activation. As platelet lipids are major membrane constituents and have an overall effect on activation [20,21], determination of the impact of shear on the composition and release of platelet lipids is vital to advance understanding of the pathophysiology of shear mediated platelet activation (SMPA).…”

Section: Introductionmentioning

confidence: 99%

Shear-Mediated Platelet Activation is Accompanied by Unique Alterations of Platelet Lipid Profile

Sweedo

Wise

Roka‐Moiia

et al. 2021

Preprint

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Platelet activation by mechanical means such as shear stress, is a vital driver of thrombotic risk in implantable blood-contacting devices used in treatment of heart failure. Lipids are essential in platelets activation and have been studied following biochemical activation. However, little is known regarding lipid alterations occurring with mechanical – shear mediated platelet activation. Here, we determined if shear-activation of platelets induced lipidome changes that differ from those associated with biochemically-mediated platelet activation. We performed high-resolution lipidomic analysis on purified platelets from four healthy human donors. For each donor, we compared the lipidome of platelets that were non-activated or activated by shear, ADP, or thrombin treatment. We found that shear activation altered cell-associated lipids and led to the release of lipids into the extracellular environment. Shear-activated platelets released 21 phospholipids and sphingomyelins at levels statistically higher than platelets activated by biochemical stimulation. Many of the released phospholipids contained an arachidonic acid tail or were phosphatidylserine lipids, which have procoagulant properties. We conclude that shear-mediated activation of platelets alters the basal platelet lipidome. Further, these alterations differ and are unique in comparison to the lipidome of biochemically activated platelets. Our findings suggest that lipids released by shear-activated platelets may contribute to altered thrombosis in patients with implanted cardiovascular therapeutic devices.

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