Faculty: Health, Medicine and Social Care
Supervisors: Dr Marcus Ilg; Dr Alice Lapthorn; Prof Selim Cellek
Location: Chelmsford
The interview for this project is expected to take place on Friday 19 April.
Apply online by 3 March 2024Fibrosis is the cause of 45% of mortality in the Western world and is defined as the excessive accumulation of extracellular matrix in response to injury. Treatment options are currently limited, with only two drugs available, both approved for the treatment of lung fibrosis.
Fibrosis is the result of dysregulated wound healing, where functional tissue is replaced with non-functional extracellular matrix and whilst this is particularly fatal in the vital organs (e.g. the heart or lungs), fibrosis can affect any organ or system in the body.
Fibrosis is driven by a key cell type called fibroblasts, which upon injury, transform into myofibroblasts. During wound healing and fibrosis myofibroblasts are responsible for the excessive production of extracellular matrix.
Extracellular vesicles (EVs) are small particles released by cells and have gained attention in fibrosis research as they can carry molecules that influence fibrosis development. Some EVs activate fibroblasts and promote excessive extracellular matrix production, contributing to fibrosis. Others play roles in inflammation and tissue repair.
We have recently discovered that EVs derived from Peyronie’s disease-derived myofibroblasts can prevent myofibroblast transformation in vitro. Specifically, we have identified the multifunctional protein TSG-6 (Tumour Necrosis Factor-α-Stimulated Gene-6) as a key mediator of this effect.
Our discovery marks the first instance in which myofibroblast-derived EVs have been implicated in exerting an anti-fibrotic effect through TSG-6.
This project seeks to provide compelling evidence of TSG-6's pivotal role in promoting fibrosis resolution and may pave the way for innovative anti-fibrotic treatments.
To accomplish these objectives, we propose an integrative approach that combines genomic, transcriptomic, proteomic and secretomic analyses.
Additionally, we intend to apply genetic modification techniques to fibroblasts and myofibroblasts obtained from patients affected by various fibrotic conditions.
This project represents a pioneering effort in the field of fibrosis research, as it marks the first comprehensive analysis that integrates these cutting-edge techniques on such a scale.
The candidate will be working as part of ARU's Fibrosis Research Group. This project will use state-of-the-art cell and molecular techniques.
The ideal candidate will have a background in cell and molecular biology.
If you would like to discuss this research project, please contact Marcus Ilg: [email protected]
Apply online by 3 March 2024The successful applicant for this project will receive a Vice Chancellor’s PhD Scholarship which covers the tuition fees and provides a UKRI equivalent minimum annual stipend for three years. For 2023/4 this was £18,622 per year. The award is subject to the successful candidate meeting the scholarship terms and conditions. Please note that the University asserts the right to claim any intellectual property generated by research it funds.