Epidural Abscess Formation as a Complication of Femoropopliteal Bypass Graft Infection

Parry, D.J.; Giles, Mitchell H.; Souka, H.; Aldoori, M I

doi:10.1053/ejvs.2000.1094

Cited by 3 publications

(1 citation statement)

References 4 publications

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“…It is demonstrated that inhibiting VWF-GPIbα interaction can reduce effectively the force-induced platelet P-selectin translocation (Goto et al, 2000;Rahman and Hlady, 2021), while VWF-GPIbα signaling through PI3K/Akt participated in platelet integrin activation and high shear stress-induced platelet P-selectin translocation (Spater et al, 2018;Chen et al, 2019;Kral-Pointner et al, 2019). It is believed that catch-slip bond transition governs the interaction of VWF with GPIbα and retains but shifts the shear stress threshold in the cases of type 2B or 2M VWF mutations that result in bleeding disorders (Coburn et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Shear Stress Accumulation Enhances von Willebrand Factor-Induced Platelet P-Selectin Translocation in a PI3K/Akt Pathway-Dependent Manner

Fang

Sun

Liu

et al. 2021

Front. Cell Dev. Biol.

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Platelet adhesion and activation through the interaction of von Willebrand factor (VWF) with platelet glycoprotein (GP) Ibα are the early key events in hemostasis and thrombosis especially under high blood shear stress. P-selectin translocation from α granule to the cell surface is a typical platelet function phenotype, which makes the platelet-induced inflammatory response of flowing leukocytes possible and can be induced by either chemical agonists (thrombin, ADP, etc.) or high blood shear stress, but regulations of VWF mutation and blood shear stress on VWF-induced P-selectin translocation remain unclear. With flow cytometry, parallel plate flow chamber, and immunofluorescence staining techniques, we examined the P-selectin translocation of platelets on immobilized wild-type (WT) VWF-A1 domain and its two mutants, the gain-of-function (GOF) mutant R1308L and the loss-of-function (LOF) mutant G1324S, respectively. The results showed that the VWF-A1-induced platelet P-selectin translocation was triggered, accelerated, and enhanced by fluid shear stress and could be correlated with shear stress accumulation (SSA, the product of fluid shear stress and mechanical stimulus time), and the PI3K/Akt axis was involved in the platelet P-selectin translocation. The force-triggered P-selectin translocation occurred quickly on partial platelet surface first and then extended gradually to the whole platelet surface as SSA increased. The P-selectin translocation process would be promoted by the GOF mutation (R1308L) but slowed down by the LOF mutation (G1324S). These findings demonstrated a force-enhanced regulation mechanism for the VWF-induced platelet P-selectin translocation through the PI3K/Akt pathway and provided a novel insight into the mechano-chemical regulation mechanism for the key events, such as platelet activation and functional phenotype change in hemostasis and thrombosis.

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