Exosomes from hypoxia-pretreated adipose-derived stem cells attenuate ultraviolet light-induced skin injury via delivery of circ-Ash1l.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background An increasing number of studies have reported that exosomes from adipose-derived stem cells (ADSCs) have antioxidant and anti-inflammatory properties. In the present study, we aimed at elucidating the potential therapeutic mechanism underlying ADSC exosomes in ultraviolet B-light (UVB)-induced skin injury. Methods We isolated the exosomes from ADSCs and hypoxia-pretreated ADSCs. High-throughput sequencing was applied to identify differential circRNA expression. Then, a UV-induced murine skin injury model was constructed and the therapeutic effect of exosomes was determined using immunofluorescence and ELISA. The regulatory mechanism was demonstrated using luciferase reporter analysis and an in vitro experiment. Results Exosomes from hypoxia-pretreated ADSCs inhibited UVB light-induced vascular injury by reversing ROS and inflammatory factor expression. High-throughput sequencing showed that exosomes from hypoxia-pretreated ADSCs (HExo) improved UV-induced skin damage via delivery of circ-Ash1l. Downregulation of circ-Ash1l inhibited the therapeutic effect of HExo on UV-induced skin damage. It was further shown that GPX4 and miR-700-5p were circ-Ash1l downstream targets. MiR-700-5p overexpression or GPX4 downregulation inhibited the circ-Ash1l protective effects of UV-induced endothelial progenitor cell (EPC) damage. Conclusion Thus, exosomes from hypoxia-pretreated A

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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