Advance description
Neutrophil depletion and deregulation are directly linked to development of diabetic foot ulcers (DFU). Scientists used a streptozotocin-treated hyperglycemic (high blood glucose/sugar) mouse model to study how overexpression of SOX2 in the skin affects wound healing. The researchers found that the combination of SOX2 upregulation and hyperglycemia in skin cells called keratinocytes triggers a pro-healing signature and increased neutrophil migration. The results highlight SOX2-mediated gene expression as a potential means of addressing neutrophil depletion in DFU.
What is exciting about this article?
Understanding the molecular changes that lead to keratinocyte activation, immune cell homing, and enhanced wound healing can be used to explore potential therapeutic targets for DFUs in humans. Results from this study implicate genes regulated by SOX2 as potential therapeutic targets for DFU treatment.
Grant support
ZIA AR041124 (Morasso, Maria) Regulation of Epidermal Differentiation
Research Areas:
Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.