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Near-infrared radiation causes sebaceous gland enlargement along with an ROS-dependent augmentation of epidermal growth factor receptor expression in hamsters. | LitMetric

AI Article Synopsis

  • NIR radiation, found in sunlight and linked to skin aging, is shown to promote sebaceous gland enlargement and skin thickening in hamsters.
  • The study reveals that this enlargement results from an increase in sebocyte proliferation, evidenced by higher levels of specific proteins (PCNA and lamin B1).
  • Additionally, NIR exposure boosts epidermal growth factor receptor (EGFR) production in sebocytes through a process that involves reactive oxygen species (ROS), with hydrogen peroxide further enhancing EGFR mRNA levels.

Article Abstract

As near-infrared radiation (NIR), which is a composition of sunlight with an 780-1400 nm wavelength, is associated with skin aging such as wrinkles and slacks, the biological actions of NIR with high dermal penetration remains unclear. In the present study, we found that NIR irradiation (40 J/cm ) at different levels of irradiance (95-190 mW/cm ) using a laboratory device with a xenon flash lamp (780-1700 nm) caused sebaceous gland enlargement concomitantly with skin thickening in the auricle skin of hamsters. The sebaceous gland enlargement resulted from the proliferation of sebocytes due to an increase in the number of proliferating cell nuclear antigen (PCNA)- and lamin B1-positive cells in vivo. In addition, NIR irradiation transcriptionally augmented the production of epidermal growth factor receptor (EGFR) accompanied with an increase in the reactive oxygen species (ROS) level in hamster sebocytes in vitro. Furthermore, the administration of hydrogen peroxide increased the level of EGFR mRNA in the sebocytes. Therefore, these results provide novel evidence that NIR irradiation causes the hyperplasia of sebaceous glands in hamsters by mechanisms in which EGFR production is transcriptionally augmented through ROS-dependent pathways in sebocytes.

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Source
http://dx.doi.org/10.1111/exd.14878DOI Listing

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