Diabetes comes with many complications, and the most debilitating of them are wounds on the feet or legs. There are an estimated 25 million Americans with diabetes, and approximately 15% of diabetics will develop an ulcer on the feet or lower legs at some point. This is because diabetes causes poor blood circulation, which lowers the efficiency of oxygen-carrying red blood cells. Without sufficient oxygen, a wound will not heal as well.
In addition, many diabetics develop a complication called neuropathy. Patients with this condition often lose feeling in their feet, making it difficult to notice a new blister or wound. Because they don’t feel any changes to the wound, it can progress in severity and even become infected, further complicating healing. Diabetic wounds, once formed, can persist for weeks and months. This leaves the patient at risk for dangerous infections—not to mention the day-to-day discomfort of an open wound.
Park Crescent‘s advanced wound care center treats a range of complicated wounds with excellent results. Now, they may soon have another tool in their arsenal, after an exciting discovery by Yale researchers.
Study Uncovers At-Fault Protein
The study, conducted by Yale doctoral student Britta Kunkemoeller, found a particular protein that maintains wounds. The protein, thrombospondin-2 (TSP2), is found in significantly higher levels in diabetic wounds. The researchers hypothesized that targeting TSP2 could potentially reverse its effects and promote wound healing.
“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,” said Kunkemoeller
TSP2 is one component of a collection of molecules—called the extracellular matrix—that serves as the foundation of cells. TSP2 influences the structure of the matrix, as well as the development of other cells within the matrix. The study found that this important protein delays wound healing.
The researchers also studied how the body produces TSP2, and discovered that TSP2 production is linked to high blood sugar levels. This explains why diabetic wounds showed higher levels of the protein.
The next stage in Kunkemoeller’s study is to develop engineered biomaterials that lack TSP2. “Our plan is to apply such materials to diabetic wounds in mouse models in order to evaluate their efficacy. Going forward, additional research will focus on either preventing the production or inhibiting the function of TSP2 in diabetic wounds.”