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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 8 (1999), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Disruption of the permeability barrier elicits a homeostatic repair response which rapidly restores barrier function while repeated barrier perturbation results in cutaneous pathology. In response to barrier disruption there is a marked increase in epidermal TNF-α and IL-1 production. To determine the potential role of TNF and IL-1 in mediating the cutaneous changes that occur following barrier disruption we compared the kinetics of barrier recovery and the degree of epidermal hyperplasia and cutaneous inflammation in TNF type I (p55) receptor and IL-1 receptor type I (p80) deficient mice. No abnormalities in epidermal morphology were observed with light or electron microscopy in receptor deficient mice. Under baseline conditions epidermal barrier function was unchanged in receptor deficient mice. Following barrier disruption the kinetics of barrier recovery were similar in control vs TNF receptor deficient mice regardless if the barrier was disrupted by acetone treatment, SDS treatment, or tape stripping. In contrast, barrier recovery was slightly but significantly accelerated regardless of the method of barrier disruption in IL-1 receptor deficient mice. The degree of epidermal hyperplasia and cutaneous inflammation following repeated barrier disruption was similar in control, TNF receptor, and IL-1 receptor deficient mice. The present study demonstrates that barrier recovery is not delayed and the degree of epidermal hyperplasia and inflammation are not altered in either TNF receptor or IL-1 receptor deficient mice, indicating that neither TNF nor IL-1 alone are essential for either barrier repair or the cutaneous pathology induced by barrier perturbation. Whereas the increase in IL-1 following barrier disruption may delay components of the repair response, whether either TNF-α or IL-1 regulate aspects of the homeostatic response remains unresolved.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 11 (2002), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Acute disruption of the cutaneous permeability barrier with either solvents or tape-stripping stimulates a homeostatic metabolic response in the subjacent nucleated layers of the epidermis that results in a rapid restoration of normal permeability barrier function. When the aged epidermal permeability barrier is stressed, it reveals a diminished capacity for recovery, in comparison to young epidermis, analogous to other organs in the aged when stressed. Although the signals that regulate this homeostatic response by the epidermis have not yet been resolved, acute permeability barrier disruption stimulates release of prestored IL-1α, and increased production of potentially regulatory cytokines, including IL-1α and TNFα in the epidermis. In these studies, we addressed the hypothesis that cytokine dysregulation explains the permeability barrier abnormality in aged epidermis, assessing the regulation of IL-1 and TNF signaling in aged vs young mice. To determine whether the IL-1 family of cytokines plays a key role in the permeability barrier abnormality of the aged, permeability barrier recovery rates were compared in transgenic mice lacking the functional IL-1 type 1 receptor vs wild-type mice at various ages. Knockout of the IL-1 type 1 receptor exacerbates the defect in permeability barrier homeostasis that is seen in age-matched, wild-type counterparts. Furthermore, the sluggish permeability barrier recovery in aged epidermis is associated with, and at least in part attributable to, altered expression of the IL-1 family of cytokines and receptors both under basal conditions and after acute barrier perturbations. Whereas modulations in cytokine expression with epidermal permeability barrier perturbation are qualitatively similar in aged epidermis, they greatly differ quantitatively. In contrast, examination of TNFα mRNA and protein basally, and following barrier perturbation revealed no alterations in aged epidermis. Together, these results show that selective alterations in the IL-1 family of cytokines occur with aging and that defects in IL-1 signaling may contribute to the epidermal permeability barrier abnormality of aged skin.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 27 (1971), S. 116-118 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 29 (1973), S. 212-213 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Zusammenfassung In Zellkulturen menschlicher Leukocyten wurden nach Stimulation zur Blasten-Transformation elektronenmikroskopische Verbindungen zwischen sich berührenden Zellen nachgewiesen, die wahrscheinlich dem Übertritt spezifischer Plasmabestand dienen.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-069X
    Keywords: X-Linked ichthyosis ; Stratum corneum lipids ; Desquamation ; Cholesterol-cholesterol sulfate:fatty acid interactions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Whereas the stratum corneum contains large amounts of unesterified cholesterol and minimal amounts of cholesterol sulfate, in recessive X-linked ichthyosis (RXLI), levels of cholesterol decrease while cholesterol sulfate content increases. To study the molecular basis for abnormal shedding in RXLI, we compared the interaction of cholesterol and cholesterol sulfate with the free fatty acid, hexadecanoic acid, by differential scanning calorimetry (DSC). While cholesterol and the free fatty acid formed a eutectic mixture, such an interaction did not occur upon mixing of cholesterol sulfate with hexadecanoic acid. In addition, and unexpectedly, free cholesterol appeared to undergo progressive autoxidation during repeated DSC measurements at only slightly supraphysiologic temperatures. These studies may provide a molecular mechanism for the abnormal desquamation that occurs in RXLI. The regular formation of oxidation products of cholesterol observed here, if matched by equivalent molecular events in vivo, may have important implications for epidermal pathophysiology.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-069X
    Keywords: Cutaneous permeability barrier ; TNFα ; Acetone treatment ; Tape stripping ; Essential fatty acid definity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have shown that (1) epidermal TNFα mRNA levels are increased following acute disruption of the cutaneous permeability barrier; (2) this increase is maximal at 1 h and decreases to control levels by 8 h; and (3) in essential fatty acid-deficient (EFAD) mice, a chronic model of barrier perturbation, TNFα mRNA levels are also elevated several-fold over controls. In the present study we determined, using immunocytochemical procedures, epidermal TNFα protein levels following either acute of chronic barrier disruption and the localization of any increase. Frozen, paraffin and Antibed sections of skin were incubated with polyclonal anti-mouse TNFα antisera and detection was accomplished by either immunoperoxidase or fluorescence procedures. We found that (1) TNFα-immunoreactive protein was present in normal mouse epidermis, and was primarily localized to the upper nucleated layers where it displayed a diffuse cytosolic pattern; (2) acute disruption of the barrier with acetone or tape-stripping resulted in TNFα staining that was more intense throughout all of the nucleated epidermal cell layers in comparison with normal epidermis; (3) the increase in TNFα staining occurred as early as 2 h after barrier disruption; and (4) increased TNFα staining was also observed in the stratum corneum of EFAD mice. These results indicate that epidermal TNFα protein levels increase after both acute and chronic barrier disruption, and are consistent with the hypothesis that TNFα may signal and/or coordinate portions of the cutaneous response to barrier disruption.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-069X
    Keywords: Serine-palmitoyl transferase ; Sphingolipid synthesis ; Transepidermal water loss ; Barrier function ; Essential fatty acid deficiency ; Epidermal permeability barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Sphingolipids, the predominant lipid species in mammalian stratum corneum play, a central role in permeability barrier homeostatis. Prior studies have shown that the epidermis synthesizes abundant sphingolipids, a process regulated by barrier requirements, and that inhibition of sphingolipid synthesis interferes with barrier homeostasis. To investigate further the relationship between epidermal sphingolipid metabolism and barrier function, we localized sphingolipid synthetic activity in murine epidermis under basal conditions, and following acute (acetone treatment) or chronic (essential fatty acid deficiency, EFAD) barrier perturbation, using dithiothreitol and/or the staphylococcal epidermolytic toxin to isolate the lower from the outer epidermis. Under basal conditions, both the activity of serine palmitoyl transferase (SPT), the rate-limiting enzyme of sphingolipid synthesis, and the rates of3H-H2O incorporation into sphingolipids were nearly equivalent in the lower and the outer epidermis. Following acute barrier perturbation, SPT activity increased significantly in both the lower (35%;P 〈 0.05) and the outer epidermal layers (60%;P 〈 0.01). The rates of3H-H2O incorporation into each major sphingolipid family, including ceramides, glucosylceramides and sphingomyelin, increased significantly in both the lower and the outer epidermis of treated flanks after acute barrier disruption. Finally, SPT activity was modestly elevated (20%;P 〈 0.01) in the lower but not in the outer epidermis of EFAD animals. These studies demonstrate the ability of both lower and outer epidermal cells to generate sphingolipids, and that permeability barrier homeostatic mechanisms appear to differentially regulate SPT acitivity and sphingolipid synthesis in the lower and the outer epidermis in response to acute and chronic barrier perturbation. Moreover, intraepidermal sites of sphingolipid synthesis displayed distinctive differences in the localization and alterations of cholesterologenesis in response to equivalent barrier perturbations.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of inherited metabolic disease 8 (1985), S. 184-186 
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 246 (1986), S. 227-227 
    ISSN: 1432-0878
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 244 (1986), S. 385-394 
    ISSN: 1432-0878
    Keywords: Cetaceans ; Lamellar bodies ; Epidermal lipids ; Permeability barrier ; Electron microscopy ; Phocena phocena
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Biochemical and ultrastructural analysis of epidermis from the porpoise, Phocena phocena, revealed certain similarities and differences between cetaceans and terrestrial mammals. The predominant cell of cetacean epidermis, not found in normal terrestrial mammals, is a lipoker-atinocyte, which elaborates not only keratin filaments, but also two types of lipid organelles: first, lamellar bodies, morphologically identical to those of terrestrial mammals, are elaborated in great abundance in all suprabasal epidermal layers, forming intercellular lipid bilayers in the stratum corneum interstices: and second, non-membrane-bounded droplets appear and persist in all epidermal layers. Although the porpoise lipokeratinocyte morpologically resembles the sebokeratocyte of avians in certain respects, nonmembrane-bounded lipid droplets are not released into the intercorneocyte space as they are in avian stratum corneum. Whereas phospholipid/neutral lipid gradients are similar in porpoise and terrestrial mammals, PAS-positive glycoconjugates, specifically glycosphingolipids, are retained in porpoise stratum corneum, but lost from these layers in terrestrials. The novel, non-polar acylglucosyl-ceramides, which also are lost during cornification in terrestrial mammals, are retained in porpoise stratum corneum. The lipid components of porpoise lipokeratinocytes appear to subserve not only barrier function in a hypertonic milieu, but also underlie the unique buoyancy, streamlining, insulatory, and caloric properties exhibited as adaptations to the cetacean habitat.
    Type of Medium: Electronic Resource
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