Getting a cut when you have diabetes can become problematic. High blood glucose damages blood vessels, making it harder for them to heal the wound. Uncontrolled diabetes can also dull the function of nerves, meaning someone with diabetes may be less likely to notice they’ve cut themselves. These two complications together are the reason for a higher rate of amputation among people with diabetes, and for the need for frequent foot exams.
Researchers at Joslin Diabetes Center may have found a solution to this problem, by modifying the patient’s own cells to be better at wound healing. This new study used cells called fibroblasts. Fibroblasts help to create the connective tissues of the body, including new skin cells.
George King, M.D., Chief Scientific Officer at Joslin Diabetes Center and Professor of Medicine at Harvard Medical School, and his lab studied fibroblasts from two different groups: one group was made up of people who have been insulin-dependent for 50+ years (they are known as the 50 Year Medalists); the second group consisted of people without diabetes. He noticed that the cells of the people who had diabetes produced less of a protein called VEGF, short for Vascular Endothelial Growth Factor.
VEGF is responsible for stimulating the growth of new blood vessels. Having too much of it is problematic in some diabetes complications. Diabetic Retinopathy, for example, can be curbed by inhibiting the ability of VEGF to create blood vessels in the eye. Eyes are such sensitive organs that having blood vessels where they shouldn’t be leads to problems like macular edema and proliferative diabetic retinopathy.
But VEGF isn’t all bad, as the scientists saw in this new research. When a cut heals itself, it needs plenty of new blood vessels throughout the healing processes. The researchers traced the lack of VEGF in wound healing to too much of a protein called PKC-delta.
They confirmed this idea that too much PKC-delta led to too little VEGF by increasing the amount of PKC-delta in the non-diabetic fibroblasts. This led to the healthy cells acting like diabetic cells and not producing enough VEGF. When they turned down the amount of PKC-delta, the cells started behaving normally again. The researchers then transplanted the diabetic cells that had PKC-delta turned down into wounds of mice who had diabetes. And, as they hoped, the wounds healed much better.
If the same holds true in humans, this could become a viable treatment for wound healing in diabetes. Doctors could take cells from a patient, turn down the actions of PKC-delta in those cells, and put the modified cells back into the patient to improve wound healing. Because the treatment cells are derived from the patient’s own body, there would be no need for immune-suppressing drugs typical in transplant situations.