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.

Abstract

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 C57BL/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.