Gp91phox‐derived Reactive Oxygen Species/Urocortin 2/Corticotropin‐releasing Hormone Receptor Type 2 Play an Important Role in Long‐term Ultraviolet A Eye Irradiation‐induced Photoaging

Photoaging is induced by long‐term ultraviolet A ( UVA ) eye irradiation. However, the mechanism of skin damage due to UVA eye irradiation is still not well understood. In this study, we used C57 BL /6j and gp91phox knockout (gp91phox −/− ) mice for the long‐term effects of UVA irradiation. The eye or dorsal skin of the mice was locally exposed to UVA for 12 months. The reactive oxygen species ( ROS ), gp91phox, corticotropin‐releasing hormone ( CRH ), urocortin 2, and CRH receptor ( CRHR ) type 1 and type 2 levels in the brain and mast cell tryptase and histamine levels in the dorsal skin all increased after UVA irradiation. The levels of CRH , urocortin 2, CRHR type 1 and type 2 in the brain also increased more after UVA eye irradiation than after UVA skin irradiation. Moreover, photoaging of the UVA eye irradiation mice was not induced following the administration of a ROS inhibitor in the brain. In addition, in gp91phox −/− mice, photoaging by UVA eye irradiation was not induced. These results indicate that long‐term UVA eye irradiation led to increased gp91phox‐derived ROS in the brain and the increased expression of urocortin 2 and CRHR type 2, resulting in photoaging; however, further studies are needed to confirm these findings.