ESR3: Laura Menke
Influence of dietary interventions upon platelet reactivity and lipidome
Atherothrombosis (a major component to cardiovascular disease) is driven by platelet activation resulting from exposure of collagen and tissue factor within blood vessels. As platelets become activated they associate in aggregates (platelet-platelet aggregates, platelet-monocyte or platelet-neutrophil aggregates). Activated platelets produce large amounts of bioactive eicosanoids through metabolism of arachidonic acid.
Recent studies have indicated dihomo-γ-linoleic acid produces inhibition of platelet function both directly and when supplied as dietary supplement. Initial observations suggest this is due to metabolism through platelet eicosanoid pathways leading to novel hydroxyeicosatetraenoic (HETE) products. These HETE products may also interact with standard anti-platelet therapies, aspirin and P2Y12 receptor blockers, to produce an enhanced anti-thrombotic and protective effect. ESR 3 will examine the influences of dihomo-γ-linoleic acid upon platelet activation characterised by standard platelet activation assays, coupled with FACS and imaging analysis together with lipidomics.
ESR 3 will employ in vitro tests on mouse and human platelets, followed by ex vivo tests on samples taken from mice and humans receiving dihomo-γ-linoleic acid supplementation.
Centre for Translational Medicine and Therapeutics
Barts and The London, Queen Mary's School of Medicine and Dentistry
London, EC1M 6BQ
To fully characterise the benefits of dihomo-γ-linoleic acid supplementation to regulate platelet activation and support the beneficial effects of anti-platelet drugs.
- UCD, Ireland (Jan-March 2018): To perform lipidomics analyses of platelet releasates.