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Go with the flow: the why and how of cardiovascular disease

  • Full or part time
  • Application Deadline
    Friday, January 10, 2020
  • Competition Funded PhD Project (Students Worldwide)
    Competition Funded PhD Project (Students Worldwide)

Project Description

Have you ever wondered why and how cardiovascular disease and atherosclerotic plaques develop in the areas that they do? Why is it that some arteries are prone to blockage while others are protected? The answer lies with blood flow. It is the type of blood flow that a vessel experiences that will decide if a plaque is going to form or not.

This project is aimed at the student who is curious about understanding the causes of cardiovascular disease with the ultimate aim of designing novel therapies that block plaque formation. The student will have the opportunity to carry out both basic and translational research using a multi-disciplinary approach that include both in vitro and in vivo approaches in a highly collaborative and supportive environment.

Forces are important in the cardiovascular system, acting as regulators of vascular physiology and pathology. Residing at the blood-vessel interface, endothelial cells are constantly exposed to mechanical forces due to the flowing blood. One of these forces is the frictional force of shear stress that can differ depending on vessel geometry and type. These patterns can range from uniform blood flow to disturbed blood flow. Although we know that endothelial cells can sense and respond differently to different types of flow, the mechanisms by which they sense and respond to blood flow remain a mystery. Our laboratory has pioneered the studies of endothelial mechanosensing and has championed the use of a multi-disciplinary approach to this scientific problem. The focus of the proposed studentship is to identify mechanisms by which endothelial cells sense and respond to blood flow. We will focus on identifying pathways that have been shown to be linked to cardiovascular disease and, depending on the interests of the candidate, can adopt a more basic or translational focus.

This DPhil will be based at the Tzima group at the Wellcome Trust Centre for Human Genetics. We are part of a wider scientific community with expertise in cardiovascular biology and the opportunity to be co-mentored and co-supervised by other senior scientists will be made available. The student will have the opportunity to be exposed to a wide range of techniques based on the student’s individual interests that include: i) use of imaging and genetic approaches to characterize how mechanosensing affects disease intitiation and progression ; (2) applying high throughput RNA sequencing and proteomics approaches to globally dissect steps involved in disease aetiology; 3) use of bioinformatics and biochemical experimental approaches to understand the role of blood flow forces in cardiovascular disease.

As well as the specific training detailed above, students will have access to high-quality training in scientific and generic skills, as well as access to a wide-range of seminars and training opportunities through the many research institutes and centres based in Oxford.

The Department has a successful mentoring scheme, open to graduate students, which provides an additional possible channel for personal and professional development outside the regular supervisory framework. We hold an Athena SWAN Silver Award in recognition of our efforts to build a happy and rewarding environment where all staff and students are supported to achieve their full potential.

Funding Notes

Funding for this project is available to basic scientists through the RDM Scholars Programme, which offers funding to outstanding candidates from any country. Successful candidates will have all tuition and college fees paid and will receive a stipend of £18,000 per annum.

For October 2020 entry, the application deadline is 10th January 2020 at 12 noon (midday).

Please visit our website for more information on how to apply.

References

Tzima E, Irani-Tehrani M, Kiosses WB, Dejana E, Schultz DA, Engelhardt B, Cao G, DeLisser H, Schwartz MA. 2005. A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature, 437 (7057), pp. 426-31.

Mehta V and Tzima E. 2016. Cardiovascular disease: a turbulent path to plaque formation. Nature, 540 (531-532).

Collins C, Osborne LD, Guilluy C, Chen Z, O'Brien ET, Reader JS, Burridge K, Superfine R, Tzima E. 2014. Haemodynamic and extracellular matrix cues regulate the mechanical phenotype and stiffness of aortic endothelial cells. Nat Commun, 5pp. 3984.

Liu Y, Collins C, Kiosses WB, Murray AM, Joshi M, Shepherd TR, Fuentes EJ, Tzima E. 2013. A novel pathway spatiotemporally activates Rac1 and redox signaling in response to fluid shear stress. J. Cell Biol., 201 (6), pp. 863-73.

Chen Z, Givens C, Reader JS and Tzima E. 2017 Haemodynamics regulate fibronectin assembly via PECAM. Sci Rep. 7 (41223)

How good is research at University of Oxford in Clinical Medicine?

FTE Category A staff submitted: 238.51

Research output data provided by the Research Excellence Framework (REF)

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