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The molecular mechanisms underpinning individual variation in platelet function and their effect on the progression and treatment of cardiovascular disease.

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

Project Description

Platelets are small blood cells that play a vital role in the chronic and acute progression of Cardiovascular Disease (CVD). Platelets respond to a range of agonists, which are released when blood vessels are damaged, by aggregating together to form thrombi. In normal circumstances this haemostatic response prevents bleeding, but if a large thrombi form in the blood vessels of the heart or the brain it can cause a heart attack or stroke. CVD is a leading cause of death globally. In the European Union CVD causes 40% of all deaths, over 1.9 million deaths each year, and cost the EU economy €196 billion in 2009, 54% of which is due to direct health care costs accounting for 9% of total health care budgets (European Cardiovascular Disease Statistics 2012).
Over recent years drugs that stop platelets aggregating (anti-platelet drugs) have proved successful in reducing the formation of pathological thrombi and preventing heart attacks and the success of these therapies is supported by extensive clinical data. In the UK 98% of all patients with coronary heart disease receive anti-platelet therapy and 38.6 million prescriptions were made for anti-platelet drugs in England in 2013, an increase from 3.6 million in 1991, and 18.9 million in 2001 (Bhatnagar et al, Heart 2015). Thrombotic disease, however, remains a leading cause of morbidity and mortality emphasising the need for more refined, safer and more effective anti-platelet strategies. One of the major challenges to improving anti-platelet therapy is balancing anti-thrombotic potential with the risk of bleeding.
To get this balance right we need new therapeutic strategies. We need to develop new drugs, but we also need to be more precise in the way we use anti-platelet drugs and how we monitor changes in their efficacy (platelet function changes over time as patients age or with changes in lifestyle, assessing these changes and altering therapy accordingly is not currently possible).
Our work focuses on the drivers and consequences of inter-individual variation in platelet function. Within this broader remit we currently have a number of specific focuses. 1) To develop platelet function tests that either more accurately reflect the action of platelets in or that are suitable for rapid analysis of platelet function in primary care and for large scale genetic or epidemiological research. 2) To investigate the molecular mechanisms that drive inter-individual variation and maybe potential drug targets. We’re currently investigating the role ILK and the regulation of integrin β3 clustering. 3) To identify the factors that alter platelet function and their effect. We’re currently investigating the effect of age, n-3 polyunsaturated fatty acids and insulin resistance.
A project is available in our laboratory to design, test and implement novel platelet function assays to measure specific aspects of inter-individual variation, elucidate the molecular mechanisms that govern these changes, and reveal how they regulate thrombus formation in health and in pathophysiological settings.
The PhD student will join the large, vibrant platelet group in Reading and have the opportunity to learn range of techniques as well as present their work on the national and international stage.
Informal enquiries about the project should be made to Dr Jones:

Funding Notes

Home, EU and overseas students with their own financial support, or who are in the process of securing funding, are welcome to contact us at any time. Funding must cover all the costs of studying for a PhD, including tuition fees, bench fees and living costs. The University of Reading is an equal opportunities employer with a diverse and vibrant community of international PhD students.

References

Jones CI. Platelet function and ageing. Mamm Genome. 2016 Aug;27(7-8):358-66
Mazet F, Dunster JL, Jones CI, Vaiyapuri S, Tindall MJ, Fry MJ, Gibbins JM. A high-density immunoblotting methodology for quantification of total protein levels and phosphorylation modifications. Sci Rep. 2015 Nov 23;5:16995
Vaiyapuri S, Roweth H, Ali MS, Unsworth AJ, Stainer AR, Flora GD, Crescente M, Jones CI, Moraes LA, Gibbins JM. Pharmacological actions of nobiletin in the modulation of platelet function. Br J Pharmacol. 2015, 172, 4133-45.
Tannetta DS, Hunt K, Jones CI, Davidson N, Coxon CH, Ferguson D, Redman CW, Gibbins JM, Sargent IL, Tucker KL. Syncytiotrophoblast Extracellular Vesicles from Pre-Eclampsia Placentas Differentially Affect Platelet Function. PLoS One. 2015 Nov 9;10(11):e0142538.
Vaiyapuri S, Sage T, Rana RH, Schenk MP, Ali MS, Unsworth AJ, Jones CI, Stainer AR, Kriek N, Moraes LA, Gibbins JM. EphB2 regulates contact-dependent and independent signalling to control platelet function. Blood. 2015,125 720-30.
Tannetta DS, Hunt K, Jones CI, Davidson N, Coxon CH, Ferguson D, Redman CW, Gibbins JM, Sargent IL, Tucker KL. Syncytiotrophoblast Extracellular Vesicles from Pre-Eclampsia Placentas Differentially Affect Platelet Function. PLoS One. 2015 Nov 9;10(11):e0142538.
Jones CI, Sage T, Moraes LA, Vaiyapuri S, Hussain U, Tucker KL, Barrett NE, Gibbins JM. PECAM-1 inhibits platelet response to thrombin and vWF by regulating the internalisation of GPIb via AKT/GSK-3/Dynamin and integrin αIIbβ3. ATVB. 2014, 34, 1968-76
Jones CI, Tucker KL, Saskikumar P, Sage T, Kaiser WJ, Moore C, Emerson M, Gibbins JM. Integrin linked kinase regulates the rate of platelet activation and is essential for the formation of stable thrombi. Journal of Thrombosis and Haemostasis. 2014, 12, 1342-52.

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