Infrared-A (IR-A) modulates the p53 pathway and diurnal clock in human skin and subcutaneous adipose tissue in vivo.

Infrared-A (IR-A) radiation is thought to protect the skin from damage due to ultraviolet radiation and alter its carcinogenic potential, possibly by preventing keratinocyte apoptosis via p53 pathway modulation. Solar radiation, including IR-A, is a major factor in contributing to the entrainment of circadian rhythms. We examined the impacts of IR-A on the intrinsic clock and transcriptomics in individuals with different diurnal preference to understand the mechanisms by which IR-A acts in the human skin and subcutaneous adipose tissue. IR-A caused multiple gene expressional changes, mainly as immediate stress responses in 15 min, that were reversed within 24 h. IR-A irradiation increased the skin surface temperature (mean peak temperature 42.9 °C). In skin, the zinc finger proteins ZNF490 and ZNHIT2 correlated negatively with the maximum skin surface temperature. In adipose tissue, CDKN1A, which codes p21 protein, had a negative correlation with the skin surface temperature change. In the skin immunohistochemical staining, the circadian regulators CRY1 and CRY2 increased significantly 24 h after the irradiation, CRY1 already in 15 min. According to the diurnal preferences, morning-type individuals develop mostly innate immune responses, whereas evening-type of individuals had more pronounced responses through p53 pathway modulation, apoptosis, and autophagy.