Acute skin barrier disruption alters the secretion of lamellar bodies via the multilayered expression of ABCA12

Abstract

BackgroundThe skin barrier consists of multiple lipid-enriched layers, which are characterized by lamellar repeated structures within the intercellular space. Sodium lauryl sulfate is a well-known substance that can disrupt the skin barrier. The mechanisms underlying the barrier repair process, especially the influence of topical sodium lauryl sulfate treatment on lipid transport in the barrier recovery phase, remain unresolved. ObjectiveTo understand the process of reconstruction of the intercellular lipid layer of the skin after acute barrier disruption by sodium lauryl sulfate treatment in vivo. MethodsFemale hairless mice were treated with 3 % sodium lauryl sulfate. Transepidermal water loss measurement, histopathological analysis, and gene expression analysis were performed from 1 to 288 h after the topical application of sodium lauryl sulfate. Western blot analysis, immunofluorescence staining, and transmission electron microscopy analysis were performed to examine the expression level of ATP-binding cassette, sub-family A, member 12 (ABCA12), and the secretion level of lamellar bodies. ResultsWe observed rapid hyper-keratinization at the stratum corneum and the subsequent concurrent secretion of lamellar bodies into the intercellular space of the stratum corneum during the process of skin barrier recovery. ABCA12 expression associated with lipid transportation into lamellar bodies was transiently upregulated and observed in multiple layers in the upper epidermis, especially in the stratum granulosum. ConclusionThe skin reacts appropriately to maintain its barrier function by first initiating hyper-keratinization and then increasing lamellar body secretion. Activation of ABCA12 is an essential factor for the recovery of skin barrier function.