Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing

Abstract Ceramide (Cer) release from glucosylceramides (GlcCer) is critical for the formation of the skin permeability barrier. Changes in β-glucocerebrosidase (GlcCer’ase) activity lead to diminished Cer, GlcCer accumulation and structural defects in SC lipid lamellae; however, the molecular basis...

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Autores principales: Michaela Sochorová, Klára Staňková, Petra Pullmannová, Andrej Kováčik, Jarmila Zbytovská, Kateřina Vávrová
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/ec2786da6eb34f7a8a0b6fe5e380cd79
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spelling oai:doaj.org-article:ec2786da6eb34f7a8a0b6fe5e380cd792021-12-02T16:08:10ZPermeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing10.1038/s41598-017-06990-72045-2322https://doaj.org/article/ec2786da6eb34f7a8a0b6fe5e380cd792017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06990-7https://doaj.org/toc/2045-2322Abstract Ceramide (Cer) release from glucosylceramides (GlcCer) is critical for the formation of the skin permeability barrier. Changes in β-glucocerebrosidase (GlcCer’ase) activity lead to diminished Cer, GlcCer accumulation and structural defects in SC lipid lamellae; however, the molecular basis for this impairment is not clear. We investigated impaired GlcCer-to-Cer processing in human Cer membranes to determine the physicochemical properties responsible for the barrier defects. Minor impairment (5–25%) of the Cer generation from GlcCer decreased the permeability of the model membrane to four markers and altered the membrane microstructure (studied by X-ray powder diffraction and infrared spectroscopy), in agreement with the effects of topical GlcCer in human skin. At these concentrations, the accumulation of GlcCer was a stronger contributor to this disturbance than the lack of human Cer. However, replacement of 50–100% human Cer by GlcCer led to the formation of a new lamellar phase and the maintenance of a rather good barrier to the four studied permeability markers. These findings suggest that the major cause of the impaired water permeability barrier in complete GlcCer’ase deficiency is not the accumulation of free GlcCer but other factors, possibly the retention of GlcCer bound in the corneocyte lipid envelope.Michaela SochorováKlára StaňkováPetra PullmannováAndrej KováčikJarmila ZbytovskáKateřina VávrováNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-8 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Michaela Sochorová
Klára Staňková
Petra Pullmannová
Andrej Kováčik
Jarmila Zbytovská
Kateřina Vávrová
Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
description Abstract Ceramide (Cer) release from glucosylceramides (GlcCer) is critical for the formation of the skin permeability barrier. Changes in β-glucocerebrosidase (GlcCer’ase) activity lead to diminished Cer, GlcCer accumulation and structural defects in SC lipid lamellae; however, the molecular basis for this impairment is not clear. We investigated impaired GlcCer-to-Cer processing in human Cer membranes to determine the physicochemical properties responsible for the barrier defects. Minor impairment (5–25%) of the Cer generation from GlcCer decreased the permeability of the model membrane to four markers and altered the membrane microstructure (studied by X-ray powder diffraction and infrared spectroscopy), in agreement with the effects of topical GlcCer in human skin. At these concentrations, the accumulation of GlcCer was a stronger contributor to this disturbance than the lack of human Cer. However, replacement of 50–100% human Cer by GlcCer led to the formation of a new lamellar phase and the maintenance of a rather good barrier to the four studied permeability markers. These findings suggest that the major cause of the impaired water permeability barrier in complete GlcCer’ase deficiency is not the accumulation of free GlcCer but other factors, possibly the retention of GlcCer bound in the corneocyte lipid envelope.
format article
author Michaela Sochorová
Klára Staňková
Petra Pullmannová
Andrej Kováčik
Jarmila Zbytovská
Kateřina Vávrová
author_facet Michaela Sochorová
Klára Staňková
Petra Pullmannová
Andrej Kováčik
Jarmila Zbytovská
Kateřina Vávrová
author_sort Michaela Sochorová
title Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
title_short Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
title_full Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
title_fullStr Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
title_full_unstemmed Permeability Barrier and Microstructure of Skin Lipid Membrane Models of Impaired Glucosylceramide Processing
title_sort permeability barrier and microstructure of skin lipid membrane models of impaired glucosylceramide processing
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/ec2786da6eb34f7a8a0b6fe5e380cd79
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