Grant: Undergraduate: Summer Studentship Award - Institute Community Support

Scar formation is an undesirable outcome of wound healing whether due to accidental trauma or surgery. Not only are scars physically unappealing, they also are associated with psychological distress and numerous morbidities, including pain and limitation on mobility, that impact millions of individuals in society. Currently, no consistent and reliable remedies are available to treat scars, thus increasing the sense of urgency to better understand wound healing in hopes of developing therapeutic solutions. The proposed study is a subproject of a larger research theme in the laboratory where we have shown that human oral gingival wounds heal faster and result in significantly less scarring than skin wounds. Thus, comparison of gingival and skin wound healing may help to find novel ways to prevent scar formation in skin. The different outcome in wound healing between these tissue types is thought to be attributed to a distinct population of fibroblasts, a type of cell that synthesizes and deposits the critical components comprising scar tissue. Data from our lab has revealed a unique population of fibroblasts in the skin, identified by a cell surface marker named CD26, which is largely absent in the gingiva. By using cultured fibroblasts, the purpose of this study is to find out how CD26 may drive scar formation. Based on the findings new drugs could be designed to suppress the scarring process. Such drugs could have important clinical applications in the treatment of burn wounds and other traumatic injuries that often lead to severe scars.