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MASTERS BY RESEARCH PROJECT: The underlying mechanism by which hypoxia regulates platelet hyperactivity

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

Project Description

Start 23 September 2019

This MSc by Research is a laboratory-based project which offers the exciting opportunity to spend 1 year in one of our State-of-the-Art laboratories (plus 1 year thesis writing) at the University of Bristol and experience life as a researcher. You will be working with one of our cutting-edge research groups where you will learn new skills and techniques, including experimental design and implementation, data analysis and scientific writing.

Platelets are small blood cells that are not only important in hemostasis but also contribute to thrombosis. Conversely, ischemic conditions such as myocardial infarction, peripheral artery disease and stroke are associated with platelet hyperactivity and reduced effectiveness of anti-platelet drugs. Recent studies showed an altered platelet protein profile in patients and animal models with ischemic disease and in platelets left under in vitro hypoxic conditions1,2. These alterations coincided with increased platelet activity. The underlying mechanism by which hypoxia can regulate platelet function however is still largely unknown. We previously showed that enhanced signalling through the PI3kinase and ERK pathways leads to platelet hyperactivity3-5. Here we hypothesise that hypoxia induces an alteration in platelet signalling pathways, resulting in platelet hyperactivity upon reoxygenation and reduced responsiveness to anti-platelet drugs. In this project the student will evaluate the effect of hypoxia on (i) intracellular signalling pathways and platelet function, and (ii) the effectiveness of anti-platelet drugs. This will be tested by using a hypoxia chamber incubating human blood/platelets under normoxic (21% O2) or hypoxic (5% O2) conditions. Platelet function will be assessed using a range of approaches, all well established in the Hers lab. The student will be trained in phlebotomy, platelet isolation and a range of functional essays including platelet aggregation, integrin activation, granule secretion, Ca2+ mobilisation and in vitro thrombosis. Techniques such as immunoprecipitation, western blotting, confocal microscopy, plate-reader based essays, FACS analysis and use of flow chambers.

Please visit the UOB/faculty of Life Sciences/ School of Physiology, Pharmacology and Neuroscience/ postgraduate studies website for the complete list of available MSc by Research projects.

Funding Notes

This is a one-year, self-funded Masters (MSc) by research. Fees are £4300 (UK/EU Fee) and bench costs are £5000. Applicants should have (or expect to receive) the equivalent of a First or Upper second-class honours degree in a biomedical discipline.

When applying please select the Faculty of Life Sciences, MSc by Research, School of Physiology, Pharmacology and Neuroscience

References

1. Cameron, S.J., et al. Hypoxia and Ischemia Promote a Maladaptive Platelet Phenotype. Arterioscler Thromb Vasc Biol 38, 1594-
1606 (2018).
2. Tyagi, T., et al. Altered expression of platelet proteins and calpain activity mediate hypoxia-induced prothrombotic phenotype. Blood
123, 1250-1260 (2014).
3. Blair, T.A., Moore, S.F. & Hers, I. Circulating primers enhance platelet function and induce resistance to antiplatelet therapy. J
Thromb Haemost 13, 1479-1493 (2015).
4. Blair, T.A., et al. Phosphoinositide 3-Kinases p110alpha and p110beta Have Differential Roles in Insulin-Like Growth Factor-1-
Mediated Akt Phosphorylation and Platelet Priming. Arteriosclerosis, thrombosis, and vascular biology (2014).
5. Blair, T.A., et al. Phosphoinositide 3-kinase p110alpha negatively regulates thrombopoietin-mediated platelet activation and thrombus
formation. Cell Signal 50, 111-120 (2018).

Related Subjects

How good is research at University of Bristol in Biological Sciences?

FTE Category A staff submitted: 64.60

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

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