Dr Jenny Dewing
University of Southampton
Jenny Dewing is working on a Retina UK-funded project with Dr Arjuna Ratnayaka at the University of Southampton. They are investigating how faults in the TIMP3 gene cause Sorsby Fundus Dystrophy (SFD), an inherited retinal disease that leads to deteriorating night vision and eventually to severe visual impairment.
The protein encoded by the TIMP3 gene has many important functions and is crucial to the health of the retinal pigment epithelium (RPE), a carpet of cells that lie underneath the photoreceptors in the retina to provide nourishment and support. It is not fully understood how faulty TIMP3 contributes to retinal degeneration in SFD, so Dr Dewing and Dr Ratnayaka are creating a cell-based model of the RPE to provide some answers and investigate potential approaches to treatment. Here, Dr Dewing tells us more about her work, her motivations, and challenges.
“When I saw the advert for Dr Ratnayaka’s post-doc position, I was very excited as it felt like the perfect project for me, making use of all the skills I had developed through my PhD in stem cell biology and two subsequent research assistant posts. The Vision group at the University of Southampton has an excellent reputation and collaboration between clinical and laboratory-based team members makes for exciting research that is extremely valuable to patients.
“On a personal level, my mum is living with glaucoma, so having the opportunity to learn more about the retina and conduct research investigating how different retinal problems lead to sight loss was really appealing.
“The cell-based model we have designed provides a scalable system to help us understand the causes of SFD at a molecular level. It has some key advantages over animal models, including the increased range and ease of control we have over the levels of normal or faulty TIMP3 in the retinal pigment epithelium cells. Whilst animal models still have an important role in research, they are sometimes limited by how comparable they are to the human system. For example, the mouse retina does not have a macula, which in humans is the part of the retina responsible for central, high-resolution colour vision, and is the site of key disease processes in many conditions, including SFD.
“The first year of the project has been focused on laying some groundwork, developing the system for generating the cell model and creating a packaging system (also known as a vector) to carry the faulty gene into the cells. Fortunately, I really enjoy this part of the work and I find it very satisfying to come into the lab and see that the bacterial colonies containing my vectors have successfully grown overnight.
“I also really enjoy microscopy work, as this is really the only time that you can actually ‘see’ what you are working on. Lots of laboratory work involves carefully mixing and pipetting colourless solutions and therefore all the science is in your head, but when you use a microscope, especially when you have stained the cells with antibodies that have fluorescent tags, you remember that you are working with a living entity that has its own goals and functions.
“The biggest frustration, of course, is when experiments do not work, and the biggest challenge is trying to not get too discouraged when that happens. Science is a continuous cycle of peaks and troughs, with the peaks being when you get some really exciting and interesting data, and the troughs being when nothing works and you feel like you’ve wasted a lot of time. However, I think if you can see value in your failures by learning from them, it makes the process much easier and more enjoyable.
“I really hope that my work will contribute valuable information to the field, with other scientists using the information I obtain to gain further insights into the molecular causes of SFD as well as other retinal diseases. The retinal pigment epithelium is critical in maintaining the health of the overlying light-sensitive cells, so our model may help us to better understand how RPE cell death impacts other parts of the retina; this learning could be useful for those investigating retinitis pigmentosa and other conditions.
“Importantly, I hope that families with retinal diseases, and SFD in particular, will have increased optimism that our research is making progress towards finding treatments for their condition. We have a unique link with a Southampton family affected by SFD and we are extremely grateful to them for providing us with tissue samples and financial support. In addition, I would like to say a huge thank you to the supporters of Retina UK who donate their time and money so that researchers like me can receive funding. Their generosity allows me to work on this project and also pays for essential laboratory equipment, all of which is critical to gaining new insights into the development and progression of diseases like SFD.”
With your support, we can continue to help scientists like Jenny look for treatments for inherited sight loss. For more information about studies funded by Retina UK, visit https://retinauk.org.uk/research/research-we-fund/ .