exposure to an elevated UV dose (100J/cm2) demonstrated epidermal cell death and separation of the dermis-epidermis junction (DEJ). Through evaluation of TUNEL expression, there was no significant apoptosis in a one-time 20J/cm2 exposure, but there was an observed accumulated expression in the 20J/ cm2/5x and 100J/cm2 exposure conditions (Figure 1B). Onetime and cumulative exposure of 20J/cm2 maintains identical Laminin-5 expression to untreated control tissue, while a onetime elevated UV-exposure (100J/cm2) induced interrupted Laminin-5 expression (Figure 1C). The cumulative effect of UV in regard to epidermal cell death and disruption to the DEJ aligned with changes to tissue structure in histology. The application of sunscreen prior to UV irradiation demonstrated a clear protective benefit in the 20J/cm2/5x and 100J/cm2 conditions as illustrated by the preservation of tissue morphology in H&E staining, reduction in the number of apoptotic cells and minimized DEJ disruption (Figure 1).
Molecular Changes in UV-Irradiated Tissue
To understand how different doses of UV irradiation can compromise the skin barrier, this study evaluates some of key biomarkers related to barrier function. Immunostaining against Filaggrin (Figure 2A) demonstrated that UV exposure did not negatively influence the expression at all of the doses evaluated in this study, suggesting non-obvious impact on the external skin barrier. Additionally, staining against DSG1 (Figure 3A) and Claudin 4 (Figure 3B) evaluated the impact on the adherens junctions within the stratum granulosum layer. Figure 2B illustrates a significant decrease in expression for 20J/cm2/5x and 100J/cm2/1x treatment groups but not for 20J/ cm2/1x, suggesting a cumulative and a dose-dependent effect on disrupting the adherens junctions. The tissue receiving sunscreen prior to UV irradiation showed normal level of DSG1 and Claudin 4 staining, suggesting the role of sunscreen in preventing disruption of the adherens junctions (Figure 3A and 3B). Immunostaining against TGM1 (Figure 2B) increased expression in the extreme UV condition (100J/cm2/1x), which does not hold true for the daily UV exposure condition (20J/ cm2/1x and 20J/cm2/5x). This elevated expression in the higher UV dose suggests that the skin was entering a reparative state to address the altered barrier. The increase in TGM1 induced
Molecular Changes in UV-Irradiated Tissue
To understand how different doses of UV irradiation can compromise the skin barrier, this study evaluates some of key biomarkers related to barrier function. Immunostaining against Filaggrin (Figure 2A) demonstrated that UV exposure did not negatively influence the expression at all of the doses evaluated in this study, suggesting non-obvious impact on the external skin barrier. Additionally, staining against DSG1 (Figure 3A) and Claudin 4 (Figure 3B) evaluated the impact on the adherens junctions within the stratum granulosum layer. Figure 2B illustrates a significant decrease in expression for 20J/cm2/5x and 100J/cm2/1x treatment groups but not for 20J/ cm2/1x, suggesting a cumulative and a dose-dependent effect on disrupting the adherens junctions. The tissue receiving sunscreen prior to UV irradiation showed normal level of DSG1 and Claudin 4 staining, suggesting the role of sunscreen in preventing disruption of the adherens junctions (Figure 3A and 3B). Immunostaining against TGM1 (Figure 2B) increased expression in the extreme UV condition (100J/cm2/1x), which does not hold true for the daily UV exposure condition (20J/ cm2/1x and 20J/cm2/5x). This elevated expression in the higher UV dose suggests that the skin was entering a reparative state to address the altered barrier. The increase in TGM1 induced
