Non-healing and chronic wounds represent a significant clinical problem, and the development of new therapies has been hampered by our incomplete understanding of the underlying biology. Epidermal keratinocytes resist mechanical stress through molecular scaffolding formed by intermediate filaments. My work in the Danuser lab focuses on the role of intermediate filament composition and organization during re-epithelialization and its contribution to wound healing.
Endothelial cells, which line the interior surfaces of blood vessels, form a barrier between the intravascular space and the surrounding tissue. These cells must form cell-cell contracts stable enough to prevent uncontrolled vascular leak, but also flexible enough to permit the dynamic rearrangements needed for new vessel formation during development and wound healing. My work has focused on identifying the molecular mechanisms responsible for endothelial junction plasticity and understanding how these pathways are disrupted in diseases characterized by inappropriate loss of endothelial adhesion.