Abstract
Background Human dermal fibroblasts (HDFs) are the primary cells in skin and are associated with UVB-induced skin photoaging. Adipose-derived stem cells (ASCs) have been proposed as a treatment for skin aging. The goal of this study was to investigate paracrine mechanisms by which ASCs repair HDFs damage from UVB exposure. Methods ASCs were cocultured with UVB-irradiated and nonirradiated HDFs. We compared HDF senescence, proliferation, migration, oxidative stress, and cytokine expression. In a nude mouse UVB-induced photoaging model, ASCs were injected subcutaneously, and skin samples were collected weekly between postoperative weeks 3 through 7. Histological analysis, PCR, ELISA, and immunohistochemistry were used to analyze the effect of ASCs. Results Compared with UVB-irradiated HDFs, nonirradiated HDFs showed higher proliferation and migration, reduced apoptosis, and fewer senescent cells when cocultured with ASCs. The expression of extracellular matrix-related cytokines was also regulated by ASCs. In addition, ASCs effectively reversed UVB-induced skin photoaging in vivo. We propose that ASCs more robustly coordinate healthy HDFs than UVB-damaged HDFs to repair aging skin. Conclusions ASCs improved the function of both UVB-damaged and healthy HDFs through paracrine effects. However, the impact of ASCs on healthy HDFs was greater than UVB-damaged HDFs. These findings help to elucidate the underlying mechanisms of the skin rejuvenation effect of ASCs.
Highlights
With the development of the economy and aging of the population, skin aging is receiving increased attention from plastic surgeons
These results indicate that isolated Adipose-derived stem cells (ASCs) maintained mesenchymal stem cells (MSCs) characteristics
We found that the paracrine effect of ASCs can better improve the function of Human dermal fibroblasts (HDFs) that are not exposed to Ultraviolet B (UVB) irradiation than HDFs exposed to UVB radiation, suggesting that ASC regenerative effects may function through lower dermal HDFs
Summary
With the development of the economy and aging of the population, skin aging is receiving increased attention from plastic surgeons. Matrix-degrading metalloproteinases (MMPs) are increased, degrading and changing the structure of the ECM, which accelerates the breakdown of connective tissue All of these changes result in the thinning of the dermis, enhancement of wrinkles, and loss of elasticity. The goal of this study was to investigate paracrine mechanisms by which ASCs repair HDFs damage from UVB exposure. Compared with UVB-irradiated HDFs, nonirradiated HDFs showed higher proliferation and migration, reduced apoptosis, and fewer senescent cells when cocultured with ASCs. The expression of extracellular matrix-related cytokines was regulated by ASCs. In addition, ASCs effectively reversed UVB-induced skin photoaging in vivo. We propose that ASCs more robustly coordinate healthy HDFs than UVB-damaged HDFs to repair aging skin. These findings help to elucidate the underlying mechanisms of the skin rejuvenation effect of ASCs
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