Skin Repair Signature in Hyperglycemic Wounds

Skin Repair Signature in Hyperglycemic Wounds hfabryova Wed, 11/27/2024 - 10:45 November 27, 2024 NIAMS IRP Maria I. Morasso, Ph.D. Laboratory of Skin Biology 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 Genetics and Genomics Molecular Biology and Biochemistry Skin Biology SOX2-Dependent Wound Repair Signature Triggers Prohealing Outcome in Hyperglycemic Wounds. O’Neill CG, Sawaya AP, Mehdizadeh S, Brooks SR, Hasneen K, Nayak S, Overmiller AM, Morasso MI J Invest Dermatol. 2025 Feb; 145 (2). doi: 10.1016/j.jid.2024.07.012 PMID: 39127091 Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.