Apoptotic Vesicles from Endothelial Cells Promote Endothelial Pro-genitor Cell Differentiation and Angiogenesis via miR-30a-5p Medi-ated Activation of the EGFR/PI3K/AKT/VEGF Pathway
Endothelial cells (ECs) are crucial for tissue repair and wound healing but are prone to damage and apoptosis. When tissues or blood vessels are injured, endothelial progenitor cells (EPCs) are quickly activated, home to the site, and differentiate into ECs for en-dothelial integrity restoration. Apoptotic vesicles (Apo-EVs), released during apoptosis, have been found to regulate the microenvironment, mediate intercellular communication, and participate in tissue repair, yet there's a lack of research on how EC-Apo-EVs, as intercellular communication mediators, regulate EPCs' differentiation into ECs and promote angiogenesis and wound repair. In this study, we induced EC apoptosis, ex-tracted Apo-EVs for promoting angiogenesis and wound repair. The isolated Apo-EVs showed excellent ability to promote EPC differentiation and angiogenesis in vitro and in vivo. In wound healing, Apo-EVs outperformed the positive control group. Mechanisti-cally, miR-30a-5p in Apo-EVs inhibits Promyelocytic Leukemia (PML), activating the Epidermal Growth Factor Receptor/Phosphatidylinositol 3-Kinase/Protein Kinase B/Vascular Endothelial Growth Factor (EGFR/PI3K/AKT/VEGF) pathway in EPCs and exerting biological effects. In vivo, Apo-EVs promote angiogenesis and wound healing, offering a new perspective on their role and a promising treatment for related diseases.