Blue Light Exposure Induces Changes Associated With Senescence and Skin Aging in Human Dermal Fibroblasts.

Blue light is becoming increasingly prevalent in our daily lives. However, the possible deleterious effects of blue light exposure on the skin have been largely overlooked. We have previously shown that blue light has the ability to induce mitochondrial DNA (mtDNA) damage and dysfunction in human dermal fibroblasts (HDFn). However, whether blue light is able to induce senescence in skin has yet to be investigated. Cellular senescence is a key part of the aging process and is heavily associated with an aging phenotype. Our study involved exposing HDFn to varying doses of blue light before assessing the expression of known senescence markers using both immunofluorescence and gene expression qPCR. We also assessed beta-galactosidase activity using a senescence-associated beta-galactosidase (SA β-gal) staining kit. Blue light induces increased γH2AX expression (p = ≤ 0.0001), indicating its ability to induce DNA double-strand breaks. P21, a known marker of senescence, is increased in response to blue light, as seen in both immunofluorescence and gene expression, where a 15-fold increase is reported in cells exposed to 50 J/cm2 blue light (p = ≤ 0.001). Importantly, NFκB also displayed a dose-dependent increase in expression following blue light exposure, with 25 J/cm2 (p = ≤ 0.0001) and 50 J/cm2 (p = ≤ 0.0001) inducing maximal nuclear translocation. SA β-gal activity also increased in response to blue light, with 25 J/cm2 being the minimum dose required to induce statistical significance (p = ≤ 0.01) when compared to a non-irradiated control group. Taken together, we demonstrate that blue light may have the ability to induce not only mtDNA damage but also nuclear DNA (nDNA) damage. This, combined with the increased expression of senescent markers and SA-β-gal activity, suggests that blue light could induce cellular senescence while also eliciting the bystander effect in neighboring cells due to increased NFκB nuclear translocation and associated reactive oxygen species (ROS) production. These findings emphasize the need for further research into the potential deleterious effects of senescence in skin and for future interventions to attenuate these effects.