The Therapeutic Effect Of Adipose-derived Stem Cells On Photoaging Fibroblasts

Repeated Exposure of Mouse Dermal Fibroblasts at a Sub-cytotoxic Dose of UVB Leads to Premature Senescence:a Robust Model of Cellular PhotoagingObjective:To develop a photo-damaged model of fibroblasts by repeated UVB exposure which mimic the specific cellular responses invoked by long term effect of UVB.Methods:Mouse dermal fibroblasts (MDFs) at early passage (passages 2) were exposed to a series of 4 sub-cytotoxic dose of UVB. The senescent phenotypes were detected at 24 or 48 hours after the last irradiation including cell viability, ROS generation, mitochondrial membrane potential, cell cycle, production and degradation of extracellular matrix.Results:Repeated exposure of UVB resulted in remarkable features of senescence. It effectively avoided the disadvantages of single dose such as induction of cell death rather than senescence, inadequate stress resulting in cellular self-rehabilitation.Conclusion:Our work confirms the possibility of detecting cellular machinery that mediates UVB damage to fibroblasts in vitro by repeated exposure, while the potential molecular mechanisms including cell surface receptors, protein kinase signal transduction pathways, and transcription factors remain to be further evaluation.Objective:We sought to investigate the protective effects of extracts of ADSCs (ADSCs-E), which presumably contain growth factors responsible for the therapeutic potential of stem cells, in a photoaging model we previously established.Methods:Murine dermal fibroblasts were exposed to repeated UVB irradiation and treated with ADSCs-E. Various senescent markers were evaluated and the potential mechanisms were tested.Results:The treatment of ADSCs-E resulted in a reverse cell shape and a decline in SA-β-gal positive cells. The cells treated with ADSCs-E also showed restored function in balancing the secretion and degradation of extracellular matrix. In addition, we observed pro-mitotic effect of ADSCs-E on photoaging cells counteracting the cell cycle arrest induced by UVB. We further confirmed a significant decrease in ROS generation and deactivation of acetyl-p53 in ADSCs-E treated group.Conclusions:These data lend credence to the antioxidant potential of ADSCs in skin biology, while identifying specific factors accounting for the effective therapy would be of great interest in future study.