Infrared A (IRA) radiation (760-1440 nm) is a major component of solar radiation and, similar to UVR, causes photoaging of human skin by increasing the expression of matrix metalloproteinase-1 in human skin fibroblasts. In this study, we assessed the IRA-induced transcriptome in primary human skin fibroblasts. Microarray analysis revealed 599 IRA-regulated transcripts. The IRA-induced transcriptome differed from changes known to be induced by UV. IRA-responsive genes include the categories extracellular matrix, calcium homeostasis, stress signaling, and apoptosis. Selected results were confirmed by real-time PCR experiments analyzing 13 genes representing these four categories. By means of chemical inhibitors of known signaling pathways, we showed that ERK1/2, the p38-, JNK-, PI3K/AKT-, STAT3-, and IL-6 as well as the calcium-mediated signaling pathways, are functionally involved in the IRA gene response and that a major part of it is triggered by mitochondrial and, to a lesser extent, non-mitochondrial production of reactive oxygen species. Our results identify IRA as an environmental factor with relevance for skin homeostasis and photoaging.

Solar radiation is well known to damage human skin, for example by causing premature skin ageing (i.e. photoageing). We have recently learned that this damage does not result from ultraviolet (UV) radiation alone, but also from longer wavelengths, in particular near-infrared radiation (IRA radiation, 760–1,440 nm). IRA radiation accounts for more than one third of the solar energy that reaches human skin. While infrared radiation of longer wavelengths (IRB and IRC) does not penetrate deeply into the skin, more than 65% of the shorter wavelength (IRA) reaches the dermis. IRA radiation has been demonstrated to alter the collagen equilibrium of the dermal extracellular matrix in at least two ways: (a) by leading to an increased expression of the collagen-degrading enzyme matrix metalloproteinase 1, and (b) by decreasing the de novo synthesis of the collagen itself. IRA radiation exposure therefore induces similar biological effects to UV radiation, but the underlying mechanisms are substantially different, specifically, the cellular response to IRA irradiation involves the mitochondrial electron transport chain. Effective sun protection requires specific strategies to prevent IRA radiation-induced skin damage.

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