INTRODUCTION
A healthy SC is critical in preventing water loss, maintaining relative barrier impermeability, and protecting against external aggressors.1 One of the critical compositions of SC is the lipid matrix. This matrix contains an equimolar ratio of cholesterol (CHOL), free fatty acids (FFAs), and ceramides (CERs).2 The molecular balance of the lipid matrix is strictly regulated by the lipid metabolism and acyl-chain trafficking in order to ensure the proper level of structural lipid synthesis.3 Functionally, ceramides help regulate cellular processes and maintain the barrier integrity of the skin. Specifically, ceramides contribute to proliferation, differentiation, and apoptosis processes, as well as immunological activity.4,5 Ceramides interact with other SC lipids to form multi-layered intercorneocyte matrix and control the water permeability of the skin. In skin disorders such as atopic dermatitis (AD), psoriasis, Netherton syndrome, and lamellar ichthyosis, the balance of the ceramide subclasses and the enzymes driving the lipid metabolism differ from the composition of normal skin.4,6 These alterations in the ceramides, along with changes to FFA and CER chain lengths, lead to significant perturbation of the lipid organization and disruption of skin barrier function that often clinically manifest as dry, scaly, itching, erythematous skin with excessive trans-epidermal water loss (TEWL).6–8
The skin barrier is susceptible to various exogenous factors, such as solar UV radiation. UV was shown to disrupt skin barrier integrity by increasing TEWL, while decreasing skin hydration, promoting SC and epidermal thickness, and changing lipid and protein levels and structures in various human skin models.9–11 Recently, we demonstrated that repeated UV exposures alter the expression of key barrier proteins and disrupt mechanical junctions.12 These changes were prevented by the use of a ceramide-containing sunscreen.12 In a recent clinical study, a physiological dose of UV (2MED) negatively impacted morphological organization and maturation of cells at the skin surface, which were prevented by application of a ceramide-containing sunscreen and moisturizing cream routine.13 Nevertheless, despite the growing understanding of UV-induced skin barrier damage, there is limited knowledge on the impact of UV on SC lipid organization and how it relates to skin barrier function. Therefore, the objective of this study was to investigate the impact of UV on ceramide subclass and chain length following exposure to a single and repeated UV doses on fresh ex vivo human skin and on healthy volunteers.
The skin barrier is susceptible to various exogenous factors, such as solar UV radiation. UV was shown to disrupt skin barrier integrity by increasing TEWL, while decreasing skin hydration, promoting SC and epidermal thickness, and changing lipid and protein levels and structures in various human skin models.9–11 Recently, we demonstrated that repeated UV exposures alter the expression of key barrier proteins and disrupt mechanical junctions.12 These changes were prevented by the use of a ceramide-containing sunscreen.12 In a recent clinical study, a physiological dose of UV (2MED) negatively impacted morphological organization and maturation of cells at the skin surface, which were prevented by application of a ceramide-containing sunscreen and moisturizing cream routine.13 Nevertheless, despite the growing understanding of UV-induced skin barrier damage, there is limited knowledge on the impact of UV on SC lipid organization and how it relates to skin barrier function. Therefore, the objective of this study was to investigate the impact of UV on ceramide subclass and chain length following exposure to a single and repeated UV doses on fresh ex vivo human skin and on healthy volunteers.
EXPERIMENTAL DESIGN
Ex Vivo Tissue Model
Fresh post-abdominoplasty normal human skin samples (seven
Fresh post-abdominoplasty normal human skin samples (seven
