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  • 2000-2004  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Blackwell Publishing Ltd/Inc.
    Experimental dermatology 13 (2004), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The neurotrophin (NT) family includes nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and NT-4/5. Keratinocytes synthesize and release all NTs. Keratinocytes express the low-affinity p75 receptor which binds all NTs, the high-affinity NGF receptor trkA and the NT-3 receptor trkC. By contrast, keratinocytes express only a truncated form of trkB, the BDNF high-affinity receptor. NT-3 stimulates keratinocyte proliferation. NTs other than NGF fail to protect keratinocytes from UVB-induced apoptosis. While NGF decreases upon UVB irradiation, NT-3 and NT-4 are upregulated. UVA dose dependently increases NT-3 levels. NT-3 and NGF stimulate each other release. Both fibroblasts and myofibroblasts synthesize and release all NTs, as well as their trk receptors except for trkC. p75 is more expressed in myofibroblast than in fibroblasts. NGF reduces secretion of collagen I in myofibroblasts. Myofibroblasts secrete more collagen I than fibroblasts. NGF reduces production of metalloproteinase 2 (MMP2) in myofibroblasts. Melanocytes synthesize and release all NTs. UVB irradiation upregulates the release of NT-3, while it downregulates the release of NT-4. Melanocytes express p75, which is downregulated by UVB. Melanocytes also express trkA and the extracellular domain of trkB. Taken together, these data indicate that a complex NT network exists in human skin with potential functions, partly to be determined.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background Chronic exposure to ultraviolet (UV) radiation induces changes in the skin structure which are mostly found in the superficial dermis and at the dermal–epidermal junction. Keratinocytes and fibroblasts contribute both to the synthesis and to the degradation of the molecules important for the integrity of this skin site. While several studies have reported on alterations of dermal components and of the functions of fibroblasts in vivo and in vitro after UV exposure, recent data suggested that keratinocytes could be the main skin cell type involved in the photoageing process. Objectives In this study, we analysed the expression of two keratinocyte molecules namely, β1 integrin (a proliferation marker) and involucrin (a differentiation marker) in sun-exposed and sun-protected facial skin of 16 healthy patients undergoing facial lifting. Methods Methods included histology, immunohistochemistry and quantitative reverse transcriptase–polymerase chain reaction analysis. Results Sun-exposed skin displayed the characteristic morphological and molecular features of dermal photoageing, compared with sun-protected skin, including dermal elastosis, diminished fibrillin and type VII collagen expression. Analysis of the epidermis in sun-exposed vs. sun-protected skin showed no histological differences, but dramatic changes in the expression of β1 integrin and involucrin. In sun-exposed skin, expression of β1 integrin protein by epidermal basal cells was reduced, paralleling a downregulation of β1 integrin mRNA, whereas involucrin protein expression was greatly enhanced in the superficial epidermal cell layers. Interestingly, the ratio between involucrin and β1 integrin protein expression was consistently increased in sun-exposed skin sites. Conclusions Collectively these results demonstrate that epidermal homeostasis is impaired by chronic UV exposure, and define β1 integrin expression as a molecular marker of the epidermal photoageing process.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  Photodamage is characterized by degradation of collagen and accumulation of abnormal elastin in the superficial dermis. Mast cells and macrophages, which are found in higher numbers in photoaged skin, have been implicated in this process.Objectives  To analyse the phenotype of haematopoietic-derived infiltrating cells in photodamaged skin.Methods  Chronically sun-exposed (preauricular) and control sun-protected (postauricular) skin was recovered from eight healthy subjects undergoing cosmetic surgery (facial lifting).Results  Histological analysis showed that sun-exposed skin harboured more infiltrating mononuclear cells than sun-protected skin. Cellular infiltrates were found at the periphery of areas of elastolysis around hair follicles in sun-exposed sites, whereas they were found in the interfollicular dermis around blood vessels and around hair follicles in sun-protected samples. Immunohistochemical analysis revealed an increased number of mast cells, macrophages and CD4+ CD45RO+ T cells in sun-exposed dermis as well as a higher number of CD1a+ dendritic cells in sun-exposed epidermis, compared with the sun-protected samples. Thus photoageing displays histological features of chronic skin inflammation. However, no molecular sign of inflammation was observed and we even found a decreased expression of interleukin-1β mRNA in sun-exposed compared with sun-protected sites. Furthermore, the patients' skin looked normal and did not display any clinical inflammation.Conclusions  Collectively, these data show that chronic ultraviolet irradiation induces alterations of innate immune cells which are recruited in sun-exposed skin without being activated.
    Type of Medium: Electronic Resource
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