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Defining the role of thymosin-beta4 as a novel regulator of inflammation in kidney disease


Project Description

One of the leading causes of end-stage kidney disease is damage to the glomerulus, the part of the kidney where the blood is filtered to make urine. This damage is partly caused by the build-up of white blood cells within the glomerulus, which causes inflammation. Thymosin-beta4 is a naturally-occurring protein that can reduce inflammation and it is already being tested in clinical trials for heart disease and other conditions. The aim of this study is to understand how thymosin-beta4 regulates inflammation in glomerular disease and to assess whether treatment with thymosin-beta4 could be a new therapeutic avenue for kidney patients.

The PhD student will have access to research facilities (including imaging, molecular biology, histology and tissue culture) and will acquire skills in a broad range of cell biology, molecular biology and imaging techniques. There will be opportunities to present at departmental meetings as well as at national and international conferences.

Funding Notes

This call is open to self-funded applicants or applicants with access to international scholarship schemes.

Eligibility Requirements
Candidates must have or expect to obtain a minimum upper-second class honours degree (or equivalent) or a Master’s degree at merit or distinction in Biological Sciences or a related subject area.

References

Vasilopoulou E, Riley PR, Long DA. (2018) Thymosin-4: a key modifier of renal disease. Expert Opinion on Biological Therapy. 18(sup1):185-192
Vasilopoulou E, Kolatsi-Joannou M, Lindenmeyer MT, White KE, Robson MG, Cohen CD, Sebire NJ, Riley PR, Winyard PJ & Long DA. Loss of endogenous thymosin beta4 accelerates glomerular disease. Kidney Int 90(5):1056-1070 (2016).

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