Variations in Lipids in Different Layers of Porcine Epidermis

Cox, Patrick; Squier, Christopher A.

doi:10.1111/1523-1747.ep12456872

Cited by 54 publications

(27 citation statements)

References 23 publications

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“…36], Nicolaides [37] first proposed these as being residual after utilization of more valuable, short-chain fatty acids for energy-requiring processes. Using the methods of cryostat sections and scanning densitometry, lipid concentrations may be analyzed to date in 12 consec utive epidermal layers, confirming those data obtained by Cox and Squier [38].…”

Section: Historical Perspectivesupporting

confidence: 79%

Stratum corneum Lipid Function

1991

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The stratum corneum contains a complex mixture of polar and nonpolar lipids in its intercellular spaces. These lipids, present in form of multiple lamellae, have been investigated for their role in providing the epidermal barrier to transcutaneous water loss, the selective barrier from the inside to the outside of the organism and partly the process of physiological desquamation. The composition of these lipids varies from species to species, with the body region and the degree of keratinocyte differentiation. The most undifferentiated layers of the epidermis contain typical membrane lipids, phospholipids, while more differentiated layers contain ceramides, cholesterol and free fatty acids. Essential fatty acids are essential for the maintenance of the lamellar structures and epidermal barrier function. Epidermal linoleic and arachidonic acids derive from exogenous sources. Only recently attempts have been made to elucidate the timing and regulation of epidermal fatty acid metabolism. Keratinocytes do not express a low molecular weight fatty acid binding protein like other cells active in lipid metabolism, but may employ alternative ways in fatty acid uptake and metabolism.

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Section: Historical Perspectivesupporting

confidence: 79%

Stratum corneum Lipid Function

1991

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“…2). This finding is similar to mature stratum corneum in which lamellar body-derived glycosphingolipids are presumed to be processed to ceramides upon secretion and glycosphingolipids are encountered only in trace quantities (27,29,30).…”

Section: Methodssupporting

confidence: 64%

Ontogeny of the Epidermal Barrier to Water Loss in the Rat: Correlation of Function with Stratum Corneum Structure and Lipid Content

et al. 1992

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ABSTRACT. The mammalian epidermal permeability barrier is provided by highly hydrophobic lipids forming multiple membrane bilayers within the extracellular domains of the outer, cornified cell layers. To characterize the critical events associated with barrier maturation, we correlated the emergence of a competent barrier to transepidermal water loss with development of the lamellar body secretory system, the organization of stratum corneum membrane bilayers, and the lipid composition of these membranes in the perinatal rat. The primary function of mammalian epidermis during terrestrial life is the generation and maintenance of a competent bamer

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“…Extrusion oflamellar body contents (at the stratum granulosum/SC interface) is followed sequentially by unfurling, elongation, and processing into mature lamellar bilayer unit structures (5)(6)(7). Concurrently, marked alterations in lipid composition occur, including the elimination ofglucosylceramides and the accumulation of ceramides in the SC ( 1,2,8,9). Recent studies have shown abundant levels of f3-glucocerebrosidase in murine epidermis, with the highest levels of enzyme activity occurring in the SC ( 10).…”

Section: Introductionmentioning

confidence: 99%

Consequences of beta-glucocerebrosidase deficiency in epidermis. Ultrastructure and permeability barrier alterations in Gaucher disease.

Holleran¹,

Ginns²,

Menon³

et al. 1994

J. Clin. Invest.

260

230

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Hydrolysis of glucosylceramide by j-glucocerebrosidase results in ceramide, a critical component of the intercellular lamellae that mediate the epidermal permeability barrier. A subset of type 2 Gaucher patients displays ichthyosiform skin abnormalities, as do transgenic Gaucher mice homozygous for a null allele. To investigate the relationship between glucocerebrosidase deficiency and epidermal permeability barrier function, we compared the stratum corneum (SC) ultrastructure, lipid content, and barrier function of Gaucher mice to carrier and normal mice, and to hairless mice treated topically with bromoconduritol B epoxide (BrCBE), an irreversible inhibitor of glucocerebrosidase. Both Gaucher mice and BrCBE-treated mice revealed abnormal, incompletely processed, lamellar body-derived sheets throughout the SC interstices, while transgenic carrier mice displayed normal bilayers. The SC of a severely affected type 2 Gaucher's disease infant revealed similarly abnormal ultrastructure. Furthermore, the Gaucher mice demonstrated markedly elevated transepidermal water loss (4.2±0.6 vs < 0.10 g/m2 per h). The electron-dense tracer, colloidal lanthanum, percolated between the incompletely processed lamellar body-derived sheets in the SC interstices of Gaucher mice only, demonstrating altered permeability barrier function. Gaucher and BrCBE-treated mice showed < 1% and < 5% of normal epidermal glucocerebrosidase activity, respectively, and the epidermis/SC of Gaucher mice demonstrated elevated glucosylceramide (5-to 10-fold), with diminished ceramide content. Thus, the skin changes observed in Gaucher mice and infants may result from the formation of incompetent intercellular lamellar bilayers due to a decreased hydrolysis of glucosylceramide to ceramide. Glucocerebrosidase therefore appears necessary for the generation of membranes of sufficient functional competence for epidermal barrier function. (J.

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Variations in Lipids in Different Layers of Porcine Epidermis

Cited by 54 publications

References 23 publications

Stratum corneum Lipid Function

Stratum corneum Lipid Function

Ontogeny of the Epidermal Barrier to Water Loss in the Rat: Correlation of Function with Stratum Corneum Structure and Lipid Content

Consequences of beta-glucocerebrosidase deficiency in epidermis. Ultrastructure and permeability barrier alterations in Gaucher disease.

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