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Contributing Role of Infrared-A (IRA) Radiation in Photoaging

The Anatomy of the Skin and Aging

The skin is the human body’s largest organ, responsible for providing a barrier to the external environment. The outermost layer of the skin is called the epidermis, which is continually exposed to a variety of stresses, including damage caused by the sun. The human epidermis has multiple layers, including the basal, spinous, and granular layers, as well as the stratum corneum. In particular, the primary cell type of the epidermis is the keratinocyte. Keratinocytes present in the basal layer of the epidermis proliferate and terminally differentiate into corneocytes, which are post-mitotic anucleated cells that form the stratum corneum. During the process of desquamation, corneocytes are shed from the top layers of the skin and are replaced by new corneocytes. Over time, this epidermal turnover slows, resulting in the visual effects of aging.

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Lifeline Normal Human Epidermal Keratinocytes in Photoaging Research

Exposure to sunlight and its damaging agents (ultraviolet and infrared radiation) can cause photoaging, which is the aging of the skin resulting from exposure to light, including sunlight. In a 2020 study, Shimizu and colleagues (opens in new window) set out to assess the role and mechanism of infrared-A (IRA) radiation in photoaging. Using Lifeline normal human epidermal keratinocytes (NHEKs), they first demonstrated that a physiological dose of IRA (determined to be approximately 800 J cm-2) inhibited NHEK proliferation after 2 or 3 days in a dose-dependent manner without cytotoxic effects. Further, they found that IRA-induced inhibition of NHEK cell proliferation was due to cell cycle arrest at G1, likely through decreased expression of cyclin D and CDK4 (responsible for cell cycle progression).

As the Akt/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway is a regulator of cell proliferation, the authors next investigated whether attenuation of this pathway could be responsible for the observed reduction in proliferation following IRA exposure. Indeed, after NHEKs were exposed to 800 J cm-2 IRA, phosphorylation of Akt, as well as 4E-BP1 and p70S6K (two mTORC1 targets) was decreased.

Next, the authors evaluated whether IRA could induce stress granule formation in NHEKs and whether stress granules could contribute to mTORC1 inhibition. They found that stress granules did form following exposure to IRA and that mTOR localized to these stress granules in an Akt-independent manner. Using treatment with leucine to activate mTORC1, the authors demonstrated that IRA-induced stress granule formation was responsible for the subsequent inhibition of mTORC1 activity.

Finally, the authors performed a morphological assessment of human skin equivalents that were exposed to IRA. As expected, they found that IRA exposure caused a number of morphological changes, including reduced epidermal thickening (a sign of reduced proliferation) increased stratum corneum thickness, and reduced proliferation of the basal layer.

Together, the results of this study suggest that IRA contributes to photoaging through mTORC1 inactivation and subsequent inhibition of keratinocyte proliferation.

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