Identification of Skin Multicellular Reprogramming Factors as Potential Treatment for Nonhealing Diabetic Foot Ulcers
作者
Ahmed S. Abouhashem,Sherine K. Saber,Sara Abouzekry,Mohammed Elkholy,Ahmed Moustafa,Ahmed Abdellatif,Ahmed S. Abouhashem,Ahmed A. Elbaz,Kanhaiya Singh,Chandan K. Sen,Hossam Sharara
Objective: In a complex environment such as that in a diabetic foot ulcer (DFU), multiple factors, including cross talk between distinct cell types of the affected tissue, play a significant role. We identified a transcription factor (TF) cocktail that induces a transition from nonhealing to healing states across multiple cell types. Approach: Thirty-three skin and wound single‐cell RNA‐sequencing samples (85,928 cells) from patients with diabetes with healing or nonhealing DFU were analyzed (GSE165816). The relative activity of cell type-specific TF in healing versus nonhealing DFU was compared, and the cumulative additive effect of different TF cocktails was assessed. Results: We used a cumulative additive-effect approach to identify five transcription factors, FOS Like 2, AP-1 Transcription Factor Subunit ( FOSL2) , CAMP Responsive Element Binding Protein 3 Like 1, RELB Proto-Oncogene, NF-KB Subunit, ETS Proto-Oncogene 1 ( ETS1 ), and X-Box Binding Protein 1, whose targets include 66.5% of pro-healing genes and only 12.5% of anti-healing genes across all cell types. In vascular endothelial cells, this TF panel accounted for 95% of vasculature-development genes; in myeloid cells, it regulated 85% of antimicrobial-response genes. In silico knockout of ETS1 or FOSL2 shifted cells toward nonhealing states, whereas Nuclear Receptor Subfamily 3 Group C Member 1 knockout shifted endothelial cells, fibroblasts, and myeloid cells toward healing-associated state. Innovation: This work recognizes a TF panel that is likely to have therapeutic value in promoting healing in nonhealing DFU. Conclusion: In this work, we identified a set of candidate TFs with the potential to induce a cell state transition favoring a switch from nonhealing to healing outcomes in patients with nonhealing DFU. Overall, our gene regulatory network-driven TF cocktail provides a rational blueprint for reprogramming DFU cell states and paves the way toward targeted regenerative therapies.