The role of Q10 engineering mesenchymal stem cell-derived exosomes in inhibiting ferroptosis for diabetic wound healing

• DOI: 10.1093/burnst/tkae054
• Publication Date: 2024-11-27T00:27:31Z
• Authors: Ronghua Yang; Sitong Zhou; Jie Huang; Deni Kang; Yao Chen; Xinyi Wang; Yan Shi; Zhengguang Wang
• Keywords: HaCaT; Coenzyme Q10

Abstract Background Ferroptosis plays an essential role in the development of diabetes and its complications, suggesting potential as a therapeutic target. Stem cell-derived extracellular vesicles (EVs) are increasingly being developed nano-scale drug carriers. The aim this study was to determine ferroptosis pathogenesis diabetic wound healing evaluate effects coenzyme Q10 (Q10)-stimulated exosmes derived from mesenchymal stem cells (MSCs). Methods Human keratinocytes (HaCaTs) were exposed high glucose (HG) conditions vitro mimic conditions, markers expression level acyl-coenzyme A synthase long-chain family member 4 (ACSL4) determined. Exosomes isolated control Q10-primed umbilical cord (huMSCs) characterized by tramsmission electron microscopy immunofluorescence staining. HG-treated HaCaTs cultured presence exosomes Q10-treated huMSCs (Q10-Exo) their migratory capacity analyzed. Results Q10-Exo significantly improved keratinocyte viability inhibited vitro. miR-548ai miR-660 upregulated taken up HaCaT cells. Furthermore, mimics downregulated ACSL4-inhibited enhanced proliferation migration. However, simultaneous upregulation ACSL4 reversed effects. also accelerated mouse model inhibiting ACSL4-induced ferroptosis. Conclusions promoted migration under hyperglycemic delivering miR-660. cutaneous mice repressing ACSL4-mediated