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Resolution of thrombo-inflammation through targeting of platelet inflammatory signalling

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  • Full or part time
    Prof K Naseem
  • Application Deadline
    No more applications being accepted
  • Funded PhD Project (European/UK Students Only)
    Funded PhD Project (European/UK Students Only)

About This PhD Project

Project Description

To celebrate the University's research successes, the University of Hull is offering this project supported by a full-time UK/EU PhD Scholarship or International Fees Bursary. It is one of a cluster of projects available as part of a significant investment into new and emerging areas of platelet research at Hull York Medical School's Hull campus.

Closing date: - 29th February 2016.
Studentships will start on 26th September 2016
Supervisor: Professor Khalid Naseem (contact [Email Address Removed]) with Dr Monica Arman

Inflammation is a complex process that is initiated to combat infection. Innate immune cells such as macrophages, leukocytes and dendritic cells use pattern recognition receptors (PRRs) on their surface to recognize damaged cells through their expression of danger-associated molecular patterns (DAMPs). Activation of PRRs on immune cells activates signalling cascades resulting in the release of chemical messengers such as cytokines and chemokines. In addition to established immune cells, blood platelets possess a number of proinflammatory actions including release of chemokines, cytokines and other chemicals promoting the recruitment of inflammatory cells.

Blood platelets are a group of cells that circulate and function to repair damage to the blood vessel wall through the formation of blood clots. However in heart disease platelets become hyperactive and drive pathological thrombosis that leads to myocardial infarctions (heart attacks). Emerging evidence suggests that platelet inflammatory functions require receptors that are important for innate immunity. These receptors, including scavenger and toll-like receptors (TLR), allow platelets to scan the blood for foreign microbes or damaged cells. The inflammatory functions of platelets activated upon encountering DAMPs likely evolved as part of general protection against infection. Interestingly, endogenous DAMPs including are associated with platelet hyperactivity, accelerated thrombosis and heart disease, suggesting a link between the immune function of platelets and atherothrombosis though the mechanism is not clear.

In this project you will study new mechanisms of pathobiology that focus on how blood platelets respond to DAMPs to promote inflammation and thrombosis. You will use molecular and cell biology techniques including phosphoflow cytometry, immunoprecipitation/immunblotting, ELISA, physiological thrombosis assays and high-resolution microscopy to determine how platelets response to distinct DAMPs and identify the receptor-signaling pathways involved. This is an excellent opportunity for training in basic cell and molecular biology techniques, and in the study of cellular signal transduction and systems biology. The student will join a team of three Post-doctoral Research assistants and three PhD students that utilizes multidisciplinary approaches to characterizing the molecular mechanisms regulating platelet function.

To apply for this post please click on the Apply button below.

In order to qualify for this scholarship you will require an undergraduate degree with at least a 2.1, or equivalent in a relevant subject.
Full-time UK/EU PhD Scholarships will include fees at the ‘home/EU' student rate and maintenance (£14,057 in 2015/16) for three years, dependent on satisfactory progress.

Full-time International PhD Fee Bursaries will include full fees at the International student rate for three years, dependent on satisfactory progress.
PhD students at Hull York Medical School follow modules for research and transferable skills development and gain a Masters level Certificate, or Diploma, in Research Training, in addition to their research degree.

Successful applicants will be informed of the award as soon as possible and by 30th April 2016 at the latest.

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