The Yale University research uncovered the role of a particular protein in maintaining the wounds and suggested that reversing its effects could help aid wound healing in patients with diabetes.
“We discovered that a specific protein, thrombospondin-2 (TSP2), is elevated in wounds of patients with diabetes as well as in animal models of diabetes,” said Britta Kunkemoeller. “To determine whether TSP2 contributes to delayed wound healing, we genetically removed TSP2 from a mouse model of diabetes and observed improved wound healing. Our study shows that TSP2 could be a target for a specific therapy for diabetic wounds.”
Most previous work on wound healing in diabetes has focused on the types of cells that are involved in wound healing such as immune cells, skin cells and the cells that form blood vessels. By contrast, Kunkemoeller’s research focuses on TSP2, a component of the extracellular matrix. The extracellular matrix is a meshwork that serves as the structural foundation for cells, like the scaffolding used in construction.
In addition to providing structural support, the extracellular matrix regulates processes that are important to wound healing, including the behavior of immune, skin and vessel-forming cells. TSP2 is a component of the extracellular matrix that influences how the matrix is formed, as well as the development and communication of other types of cells that grow within the matrix.
“Our focus on TSP2 therefore allowed us to study a single molecule that influences several wound-healing related processes,” explained Kunkemoeller.
The research will be presented at the American Society for Investigative Pathology annual meeting during the 2018 Experimental Biology meeting.