Abnormal expression of sphingomyelin acylase in atopic dermatitis: an etiologic factor for ceramide deficiency?

摘要: Previously, we demonstrated that there is a marked reduction in the amount of ceramide stratum corneum both lesional and nonlesional forearms atopic dermatitis (AD), suggesting an insufficiency ceramides etiologic factor dry barrier-disrupted skin. In this study, investigated, as possible mechanism involved deficiency, whether sphingomyelin (SM) metabolism altered AD compared to normal controls. stripped biopsied whole epidermis patients with AD, SM hydrolysis measured at pH 4.7 using [ choline-methyl - 14 C]sphingomyelin substrate were markedly increased by 27- 7-fold, respectively. Radio-thin-layer chromatography reaction products revealed that, whereas age-matched controls associated sphingomyelinase (SMase) degrades yield phosphorylcholine (PC), most detected attributable not SMase but hitherto undiscovered epidermal enzyme, acylase, which releases free fatty acid sphingosyl-PC (Sph-PC) instead ceramides. The potential acylase-like enzyme generate Sph-PC through was corroborated thin-layer chromatographic analysis obtained porcine kidney followed high-performance liquid chromatography-mass spectrometry. Further-more, also spectrometly after incubation samples. On other hand, contact or chronic eczema exhibited neither nor generation upon radio-thin-layer analysis. These findings suggest resulting decrease levels ceramides, could be continuous barrier disrupted skin observed AD.