Beta vulgaris-Derived Exosome-like Nanovesicles Mitigate Photoaging by Attenuating Oxidative Stress and Promoting Collagen Biosynthesis Abstract
Differential gene expression (DEG) analysis identified a total of 1,316 significantly altered genes, with 852 genes upregulated and 464 downregulated in the BVNV-treated group compared to the UVB-irradiated control group. The significant upregulation of SPRR1A, SPRR1B, and KRT17, genes known to be crucial for keratinocyte proliferation and the formation of the epidermal barrier, indicates that BVNVs actively promote the restoration of the skin's physical barrier, a key defense mechanism compromised by UV exposure. Additionally, the expression of INHBA, which encodes the ßA subunit of Activin A, was significantly increased. Activin A, a key ligand of the TGF-ß signaling pathway, is a primary regulator of collagen synthesis. This provides a strong molecular link to the promotion of dermal matrix integrity. In summary, transcriptomic analysis shows that BVNV treatment modulates a series of genes critical for skin barrier integrity, cell proliferation, and extracellular matrix (ECM) remodeling. The data reveal that BVNVs coordinate multifaceted cellular responses by simultaneously enhancing skin barrier function and driving ECM remodeling through key signaling pathways, offering new insights into how BVNVs exert protective and restorative effects on photo-damaged skin through complex molecular networks. Overall design: RNA sequencing analysis was performed on UVB-irradiated HaCaT cells and BVNV-treated UVB-irradiated HaCaT cells (n=3).