Prostacyclin reverses platelet stress fibre formation causing platelet aggregate instability.

ABSTRACT: Prostacyclin (PGI₂) modulates platelet activation to regulate haemostasis. Evidence has emerged to suggest that thrombi are dynamic structures with distinct areas of differing platelet activation. It was hypothesised that PGI₂ could reverse platelet spreading by actin cytoskeletal modulation, leading to reduced capability of platelet aggregates to withstand a high shear environment. Our data demonstrates that post-flow of PGI₂ over activated and spread platelets on fibrinogen, identified a significant reduction in platelet surface area under high shear. Exploration of the molecular mechanisms underpinning this effect revealed that PGI₂ reversed stress fibre formation in adherent platelets, reduced platelet spreading, whilst simultaneously promoti

SUBMITTER: Yusuf MZ 

PROVIDER: S-EPMC5514131 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature