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Human adipose mesenchymal stem cell derived extracellular vesicles‐delivered HSP27 alleviates UVB ‐induced photoaging

光老化 间充质干细胞 化学 皮肤老化 细胞生物学 细胞外基质 脂肪组织 流式细胞术 伤口愈合 干细胞 人体皮肤 免疫印迹 癌症研究 分子生物学 生物化学 生物 免疫学 皮肤病科 医学 遗传学 基因
作者
Qianwen Zeng,Rentao Yu,Genlong Bai,Qian Wu,Bo Chen,Aijun Chen
出处
期刊:Photochemistry and Photobiology [Wiley]
卷期号:102 (2): 418-432 被引量:1
标识
DOI:10.1111/php.70015
摘要

Skin photoaging is a skin condition caused by long-term exposure to ultraviolet radiation, especially UVA and UVB, which leads to wrinkles, pigmentation, skin sagging, and telangiectasia. Histopathologically, it is characterized by a significant reduction in dermal collagen and abnormal accumulation of elastic fibers. Preventing or ameliorating photoaging may provide a promising therapeutic approach for these changes. In recent years, multiple studies have reported the potential of mesenchymal stem cells (MSCs) in treating various skin diseases. Given that extracellular vesicles (EVs) can deliver diverse substances to receptor cells and produce therapeutic effects similar to parental cells, we aim to explore whether adipose-derived mesenchymal stem cell-derived extracellular vesicles (AMSC-EVs) can improve skin photoaging by delivering heat shock protein 27 (HSP27). The specific effects of AMSC-EVs on the photoaging model of human dermal fibroblasts (HDFs) or human immortalized keratinocytes (HaCaTs) induced by UVB irradiation were investigated through CCK-8 experiments, cell migration experiments, flow cytometry, immunofluorescence, and Western blot. Our research found that AMSC-EVs improved the survival rate and migration ability of HDFs and HaCaTs after UVB irradiation, alleviated cell senescence, reduced DNA damage, inhibited the production of ROS, and promoted the remodeling of extracellular matrix (ECM). Further research showed that after knocking down HSP27, the anti-aging/light protection ability of AMSC-EVs was significantly weakened. Overall, our data suggest that we have revealed the anti-photoaging effect of AMSC-EVs on HDFs and HaCaTs, which may be mediated by the delivery of HSP27.
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