Department of Dermatology, Northwest Hospital, The Second Affiliated Hospital of Xi'an Jiaotong University, 157 Xi Wu Road, Xi'an, 710004, Shaanxi, China.
Department of Cosmetic Dermatology, Mylike Cosmetology Hospital of Yunnan, Kunming, China.
Photochem Photobiol Sci. 2024 Jan;23(1):55-63. doi: 10.1007/s43630-023-00498-y. Epub 2023 Dec 15.
Accumulation studies have found that adipose-derived stem cell (ADSC) exosomes have anti-oxidant and anti-inflammatory characteristics. The current study verified their therapeutic potential to elucidate mechanisms of ADSC exosome actions in ultraviolet B (UVB) light-induced skin injury. Exosomes were isolated from ADSCs and hypoxic pretreated ADSCs. Next-generation sequencing (NGS) was applied to characterize differential mRNA expression. A UV-induced mice skin injury model was generated to investigate therapeutic effects regarding the exosomes via immunofluorescence and ELISA analysis. Regulatory mechanisms were illustrated using luciferase report analysis and in vitro experiments. The results demonstrated that exosomes from hypoxic pretreated ADSCs (HExos) inhibited UVB light-induced vascular injury by reversing reactive oxygen species, inflammatory factor expression and excessive collagen degradation. NGS showed that HExos inhibits UV-induced skin damage via GLRX5 delivery, while GLRX5 downregulation inhibited the therapeutic effect of HExos on UV-induced skin damage. GLRX5 upregulation increased the protective Exo effect on UV-induced skin and EPC damage by inhibiting ferroptosis, inflammatory cytokine expression and excessive collagen degradation. Therefore, the data indicate that HExos attenuate UV light-induced skin injury via GLRX5 delivery and ferroptosis inhibition.
累积研究发现脂肪来源干细胞(ADSC)外泌体具有抗氧化和抗炎特性。本研究通过验证其治疗潜力,阐明了 ADSC 外泌体在紫外线 B(UVB)光诱导皮肤损伤中的作用机制。从 ADSC 和低氧预处理的 ADSC 中分离出外泌体。应用下一代测序(NGS)对差异 mRNA 表达进行特征分析。通过免疫荧光和 ELISA 分析,建立 UV 诱导的小鼠皮肤损伤模型,研究外泌体的治疗效果。利用荧光素酶报告分析和体外实验阐明调控机制。结果表明,低氧预处理 ADSC 的外泌体(HExos)通过逆转活性氧、炎症因子表达和胶原过度降解,抑制 UVB 光诱导的血管损伤。NGS 显示,HExos 通过 GLRX5 的传递抑制 UV 引起的皮肤损伤,而 GLRX5 的下调抑制了 HExos 对 UV 引起的皮肤损伤的治疗作用。GLRX5 的上调通过抑制铁死亡、炎症细胞因子表达和胶原过度降解,增加了对外泌体对 UV 诱导的皮肤和 EPC 损伤的保护作用。因此,数据表明 HExos 通过 GLRX5 的传递和铁死亡抑制减轻 UV 光诱导的皮肤损伤。