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

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/cm2 ) at different levels of irradiance (95-190 mW/cm2 ) 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.

Different regulation of lipogenesis in sebocytes and subcutaneous preadipocytes in hamsters in vitro.

Sebaceous gland cells (sebocytes) differentiate to intracellularly accumulate lipid droplets - a phenomenon similar to that found in adipocytes. In the present study, we examined whether the regulation of lipogenesis in sebocytes is the same as that in preadipocytes. When sebocytes and preadipocytes, prepared from auricle and subcutaneous adipose tissues from the inguinal region of hamsters, respectively, were treated with a common differentiation inducer, insulin, intracellular lipid-droplet formation and triacyglycerol (TG) production were dose- and time-dependently augmented in both. Insulin increased the production of perilipin, a differentiation marker in both sebocytes and adipocytes. Insulin-like growth factor 1 (IGF-1) augmented the intracellular level of TG in sebocytes and preadipocytes. In addition, the action of 1α,25-dihydroxyvitamin D3 [1,25(OH2)D3] on TG production was the opposite between sebocytes and preadipocytes. Furthermore, 5α-dihydrotestosterone (5α-DHT) augmented the TG level in sebocytes, whereas it did not alter TG production in preadipocytes. Moreover, insulin-augmented TG production in sebocytes was enhanced by IGF-1 and 5α-DHT, while diminished by 1,25(OH2)D3. In preadipocytes, the insulin-augmented production of TG was decreased by IGF-1, 1,25(OH2)D3, and 5α-DHT. These results suggest that sebocytic lipogenesis is partially similar to but substantially different from adipocyte lipogenesis due to the forementioned hormones and growth factors in the skin under physiological conditions.