Exposure to sunlight, mainly UVA, leads to typical changes in the features of the skin known as photoaging. UVA irradiation induces the expression of proteases that are responsible for the degradation of the extracellular matrix proteins to results in photoaging; it also downregulates the expression of proteins that are needed for the skin structure. Since, it is known that cells in the neighborhood of irradiated cells, but not directly exposed to it, often manifest responses like their irradiated counterparts, it is important to evaluate if these bystander cells too, can contribute to photoaging. UVA induced cell cycle arrest has been associated with photoaging, from flow cytometry analysis we found that there was an induction of cell cycle arrest at the G1/S phase in the UVA-bystander cells. The expression of some key photoaging marker genes likes, matrix metalloproteinases (MMP-1, MMP-3, MMP-9), cyclooxygenase-2 (COX-2), collagen1 and elastin were assessed from qRT-PCR. Up-regulation of MMP-1 and COX-2, downregulation of collagen1 and elastin, along with suppression below normal expression for MMP-3 and MMP-9 was observed in the UVA-bystander A375 cells. Our findings suggest that UVA-bystander cells may contribute to the process of photoaging.
Keywords: Bystander response; Cyclooxygenase-2 (COX-2); Matrix metalloproteinase-1 (MMP-1); Photoaging; UVA.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.