Intrinsically Aged Epidermis Displays Diminished UVB-Induced Alterations in Barrier Function Associated with Decreased Proliferation

Ultraviolet (UV) irradiation of the skin induces a variety of responses in the epidermis, including sunburn cell Formation, epidermal hyperplasia, and a dose-dependent permeability barrier abnormality, an effect that appears to be dependent upon both UVB induced hyperplasia and T-cell activation. Since intrinsically aged epidermis displays decreased epidermal turnover, diminished inflammatory response to various stimuli, including UVR, and impaired immune Function, we investigated the effects of UVB on both epidermal barrier Function and proliferation in hairless mice of increasing chronologic age (27, 61, and 90 wk). After a single UVB exposure (0.15J/cm2 ≈7.5 MED), a barrier abnormality developed (i.e., increased transepidermal water loss; TEWL), after a delay of ≥48 h, regardless of age. In young mice (27 wk old), TEWL levels peaked at 72–96h (9.9-fold over untreated controls), whereas increased epidermal [3H]thymidine incorporation preceded the peak TEWL increase (i.e., ≈570% increase over controls at 48 h). In contrast, the UVB-induced increased in both TEWL and DNA synthesis were significantly diminished, with decreased epidermal hyperplasia evident, in intrinsically aged versus young mouse epidermis. Baseline epidermal thickness decreased with animal age (i.e., 16.8±3.1 vs. 27.9±0.7 μm for 90- vs. 27-wk-old animals, respectively; p