Coordinate assembly of lipids and enzyme proteins into epidermal lamellar bodies

Rassner, Ulrich; Feingold, Kenneth R.; Crumrine, Debra; Elias, Peter M.

doi:10.1054/tice.1999.0050

Cited by 63 publications

(53 citation statements)

References 37 publications

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“…Also we found round granules of 250-400 nm diameter and electron-dense cores containing fi ne granular material in the keratinocytes of stratum spinosum. These structures resembled lamellar bodies which contribute to the formation of intercellular epidermal water barrier (27)(28)(29). In this study, we observed blood capillaries with distended lumens, expansions between the collagen fi bers of connective tissue and accumulation of a homogenous material in the dermal layer of the skin with tinea pedis.…”

Section: Discussionsupporting

confidence: 54%

Ultrastructural Alterations In The Epidermis Of Patients With Tinea Pedis

Canberk¹,

Ahıshalı²,

Onar³

et al. 2009

TUTFD

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Section: Discussionsupporting

confidence: 54%

Ultrastructural Alterations In The Epidermis Of Patients With Tinea Pedis

Canberk¹,

Ahıshalı²,

Onar³

et al. 2009

TUTFD

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“…The incorporation of the lipid hydrolases and proteases into lamellar bodies requires the prior or concurrent delivery of lipid to the lamellar bodies (49). If lipids are deficient, the enzymes that are characteristically found in lamellar bodies are not transported from the Golgi to the lamellar bodies (49). Recent studies have shown that ABCA12, a member of the ABC family of transporters, is required for lamellar body formation (50,51).…”

Section: Jlr: Is Anything Known About How Lamellar Bodies Are Formed?mentioning

confidence: 99%

Thematic review series: Skin Lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis

Feingold

2007

Journal of Lipid Research

366

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The permeability barrier is required for terrestrial life and is localized to the stratum corneum, where extracellular lipid membranes inhibit water movement. The lipids that constitute the extracellular matrix have a unique composition and are 50% ceramides, 25% cholesterol, and 15% free fatty acids. Essential fatty acid deficiency results in abnormalities in stratum corneum structure function. The lipids are delivered to the extracellular space by the secretion of lamellar bodies, which contain phospholipids, glucosylceramides, sphingomyelin, cholesterol, and enzymes. In the extracellular space, the lamellar body lipids are metabolized by enzymes to the lipids that form the lamellar membranes. The lipids contained in the lamellar bodies are derived from both epidermal lipid synthesis and extracutaneous sources. Inhibition of cholesterol, fatty acid, ceramide, or glucosylceramide synthesis adversely affects lamellar body formation, thereby impairing barrier homeostasis. Studies have further shown that the elongation and desaturation of fatty acids is also required for barrier homeostasis. The mechanisms that mediate the uptake of extracutaneous lipids by the epidermis are unknown, but keratinocytes express LDL and scavenger receptor class B type 1, fatty acid transport proteins, and CD36. Topical application of physiologic lipids can improve permeability barrier homeostasis and has been useful in the treatment of cutaneous disorders.-Feingold, K. R. The role of epidermal lipids in cutaneous permeability barrier homeostasis. J. Lipid Res.

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“…The procedures used for quantifying LB density were previously described in detail ( 37 ). Briefl y, for LB quantifi cation, у 10 micrographs were taken randomly from different, nonoverlapping regions at the stratum granulosum (SG)-SC interface at 16,000× magnifi cation of each sample.…”

Section: Assessment Of Lb Density and Secretionmentioning

confidence: 99%

Regulation of ABCG1 expression in human keratinocytes and murine epidermis

Jiang

Lü

Tarling

et al. 2010

Journal of Lipid Research

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Journal of Lipid ResearchCholesterol levels are tightly regulated in cells, and maintenance of cholesterol homeostasis is of particular importance in keratinocytes/epidermis. In addition to being an essential component of all cell membranes, cholesterol is required in differentiated keratinocytes to form lamellar bodies (LBs) ( 1, 2 ). Secretion of these unique organelles delivers lipids, including cholesterol, which mediate permeability barrier function, to the extracellular spaces of the stratum corneum (SC) ( 2 ). The ability to limit the transcutaneous movement of water and electrolytes is required for terrestrial life. Although cholesterol synthesis rates are high under basal conditions, following permeability barrier disruption, epidermal cholesterol synthesis increases ( 3 ), as do the levels of receptors such as the LDL receptor and scavenger receptor class B, member 1 that enhance the uptake of cholesterol into keratinocytes ( 4, 5 ). Inhibition of cholesterol synthesis perturbs permeability barrier function ( 6 ), and a selective deficiency in cholesterologenesis largely accounts for the barrier abnormality in chronologically aged epidermis ( 7,8 ). Cholesterol is also the precursor of an important bioregulatory molecule in keratinocytes, cholesterol sulfate (CS), which regulates epidermal keratinocyte differentiation ( 9-11 ) and corneocyte desquamation by diverse mechanisms ( 12, 13 ).Abstract ABCG1, a member of the ATP binding cassette superfamily, facilitates the effl ux of cholesterol from cells to HDL. In this study, we demonstrate that ABCG1 is expressed in cultured human keratinocytes and murine epidermis, and induced during keratinocyte differentiation, with increased levels in the outer epidermis. ABCG1 is regulated by liver X receptor (LXR) and peroxisome proliferatoractivated receptor-␦ (PPAR-␦ ) activators, cellular sterol levels, and acute barrier disruption. Both LXR and PPAR-␦ activators markedly stimulate ABCG1 expression in a doseand time-dependent fashion. PPAR-␥ activators also increase ABCG1 expression, but to a lesser degree. In contrast, activators of PPAR-␣ , retinoic acid receptor, retinoid X receptor, and vitamin D receptor do not alter ABCG1 expression. In response to increased intracellular sterol levels, ABCG1 expression increases, whereas inhibition of cholesterol biosynthesis decreases ABCG1 expression. In vivo, ABCG1 is stimulated 3-6 h after acute barrier disruption by either tape stripping or acetone treatment, an increase that can be inhibited by occlusion, suggesting a potential role of ABCG1 in permeability barrier homeostasis. Although Abcg1 -null mice display normal epidermal permeability barrier function and gross morphology, abnormal lamellar body (LB) contents and secretion leading to impaired lamellar bilayer formation could be demonstrated by electron microscopy, indicating a potential role of ABCG1 in normal LB formation and

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Coordinate assembly of lipids and enzyme proteins into epidermal lamellar bodies

Cited by 63 publications

References 37 publications

Ultrastructural Alterations In The Epidermis Of Patients With Tinea Pedis

Ultrastructural Alterations In The Epidermis Of Patients With Tinea Pedis

Thematic review series: Skin Lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis

Regulation of ABCG1 expression in human keratinocytes and murine epidermis

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