Using hair follicles to source Collagen 7 to heal wounds in EB

• Primary Researcher: Prof Desmond Tobin
• Institution: University College Dublin
• Type of EB: DEB
• Funding amount: €20,000 to supplement the UCD Newman Scholarship Grant
• Project length: 2 years

Due in 2024

Desmond Tobin is a Full Professor of Dermatological Science at UCD School of Medicine and Director of the Charles Institute of Dermatology, University College Dublin. Previously he was Professor of Cell Biology and Director of the Centre for Skin Sciences (2009-2018) at University of Bradford, where he holds an Honorary Visiting Research Professorship.

Desmond was awarded a BSc from the National University of Ireland (Maynooth), a PhD from the University of London (St. John’s Institute of Dermatology) and has held post-doctoral training and Junior Faculty positions at New York University Medical School’s Department of Dermatology.

Over the past 25+ years he has researched in basic and applied skin/hair sciences, with a particular focus on the regulation of hair growth in health and disease especially those conditions with an immune-medicated basis, and on the biology of human melanocytes/pigmentation in health and disease. He hopes to now bring this wealth of knowledge to the field of EB, in the hopes of developing a suitable treatment for the condition.

Grant title: The scalp hair follicle as a source of collagen VII-positive wound healing cells in Recessive Dystrophic Epidermolysis Bullosa

Epidermolysis bullosa (EB) is a group of inherited and incurable skin disorders, where blistering/erosions can occur spontaneously or after minimal physical trauma. Chronic wounds are then complicated by infections, prolonged inflammation, and in some types, skin cancer. Currently management of EB is limited to control of pain and itch, minimisation of infection, and surgical management of complications. There is an urgent need to improve patients’ life opportunities.

In this project, we will focus on patients with Recessive Dystrophic EB (RDEB), whose skin splits in the upper dermis, and ask whether their skin can benefit from harnessing regenerative power of their (often) unaffected scalp hair follicles (HF).

Patients with RDEB carry a mutated COL7A1 gene, making them unable to produce much, if any, functioning type VII collagen. This collagen helps to hold skin together when placed under even minimal strain. Skin sites that are often protected from RDEB blistering include scalp and underarm; areas with large HF with functioning type VII collagen. The rich regenerative capacity of HF makes them excellent potential repair ‘tool-kits’ in RDEB.

Our project team has expertise in HF biology and clinical care of EB patients that is unique in Ireland. We propose in this proof-of-concept project to examine if cell-based approaches based on type VII collagen-expressing HF cells could support RDEB blisters and blister-prone skin that lacks this key collagen.
Using an array of biomolecular tools, we will compare type VII collagen status in normal healthy scalp skin and HF, and compare this with type VII collagen status in ethically-obtained scalp HF from RDEB patients.

We will examine skin and HF tissues as well as different cell types isolated from skin and HF, for insights into how best to exploit the remaining RDEB type VII collagen-expressing cells to aid skin integrity in this vulnerable patient group.

Due in 2024