Elena Drudi
Academic and Work Experience Prior to Sept 2019 Programme Start
I completed my undergraduate degree in Biomedical Engineering at Imperial College London. During my time there I became interested in how mechanical forces affect tissues in the body.
In my third-year project I looked at the effect of mechanical forces on wound repair. For my master’s project I studied the effects of mechanical forces on endothelial cells and how this relates to the activation of the Wnt signalling pathway.
PhD Programme- Year 1- MRes and Project Rotations
During my first year in the Wellcome Trust ‘Cell Therapies and Regenerative Medicine’ PhD Programme I have had the opportunity to learn many new skills:
In my first rotation with Dr Eileen Gentleman I used a novel hydrogel system to study the effect of different microenvironment stiffnesses on leukaemia cells.
In my second rotation, under the supervision of Dr Tanya Shaw, I studied the extracellular matrix composition of cancer associated fibroblasts and healthy fibroblasts. The aim was to understand if there is a link between immune response and fibrotic formation.
In my final rotation with Professor Steven Sacks and Dr Giorgia Fanelli during the UK COVID-19 lockdown, I learned how to write a review article. The review article focused on the current progress in complement inhibition-based therapy for the management of age-related macular degeneration.
PhD Programme – Years 2 to 4 – Doctoral Studies
To date, a complete mediation of scarring has not been achieved, but it is known that extracellular matrix (ECM), part of the connective tissue of the skin, is one of the main components that is changed during wound healing. Therefore, mediating the ECM might be key in reducing scarring. In the skin many different types of scars can occur, however there are some which are pathological and reduce the quality of life of patients, such as in keloid disease and recessive dystrophic epidermolysis bullosa (RDEB). Recent studies have shown that the ECM in keloids has unique characteristics compared with that from normal scars and skin. These could be similar in RDEB due to their similar fibrotic condition.
In my project I will start with transcriptional profiling to identify distinct qualities between normal skin and fibrotic skin diseases (keloids and RDEB). I will use the acquired information to run a compound screen to see if ECM can be restored to a healthy state. If successful targets have been shown to change the ECM, I will further study the specific pathways they activated. All the previous steps are using a specific technique where cells deposit their own ECM, known as cell derived matrix (CDM). The last step will compare the discovered in-vitro information to ex-vivo and in-vivo models. This will give a more conclusive picture on whether the skin is healing with a reduced amount of scarring.
