ACTL6A deficiency attenuates UV-induced cellular senescence in human dermal fibroblasts via inducing apoptosis

Background Ultraviolet irradiation (UVR) can induce both cellular senescence and cell apoptosis, which is mainly determined by the DNA damage response. The mechanism that determines the cellular outcome after UVR has not been fully illuminated. Objective To investigate the role of ACTL6A in the response of human dermal fibroblasts to UVR. Methods Human dermal fibroblasts were used to find the function and mechanism of ACTL6A in photoaging and verified in mice. Results ACTL6A expression was significantly increased both in vitro and in vivo after UVR exposure. Interference ACTL6A expression in HDFs inhibited the UVR stress-induced premature senescence, intracellular ROS production and SASP secretion. Meanwhile, knockdown of ACTL6A promotes apoptosis of senescent cells. Conclusion ACTL6A exhibited a critical role in resolving the cell fate under UVR and maybe a potential target for the therapy of UV-induced diseases and UV-needed diseases.