This study demonstrates that AMSC-derived extracellular vesicles improve cellular survival and migration in photoaged skin, indicating HSP27 as a crucial mediator.
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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Zeng et al. (2025) studied this question.
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