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  • 1
    Online Resource
    Online Resource
    Klimavorhersage und Klimavorsorge. (2002)
    Berlin, Heidelberg :Springer Berlin / Heidelberg,
    Details
    Keywords: Climatic changes-Government policy. ; Climatic changes-International cooperation. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (490 pages)
    Edition: 1st ed.
    ISBN: 9783642559815
    Series Statement: Ethics of Science and Technology Assessment Series ; v.16
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=6299293
    DDC: 363.73874526
    Language: German
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    GEOMAR EBL
  • 2
    Electronic Resource
    Electronic Resource
    Transforming growth factor-β1 and ultraviolet A1 radiation increase production of vascular endothelial growth factor but not endothelin-1 in human dermal fibroblasts (2000)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 143 (2000), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  Normal and dysregulated wound healing involves fibroblast activation and angiogenesis, in which polypeptide factors such as transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF) and endothelin-1 (ET-1) play an important part. Ultraviolet (UV) A1 (365 nm) has recently received attention as a possible treatment for some dermal fibrotic disorders. Objectives The aim of this study was to evaluate the effects of TGF-β1 and UVA1 radiation, as well as that of cobalt chloride, reported to mimic hypoxia both in vivo and in vitro, on the expression of VEGF and ET-1 by cultured human dermal fibroblasts. Methods Levels of VEGF and ET-1 were measured by enzyme-linked immunosorbent assay and expression of neutral endopeptidase (NEP, CD10), known to degrade ET-1, was quantified by flow cytometric analysis after cell trypsinization. Results Our results showed that the cells released minor amounts of VEGF and ET-1. Both TGF-β1 and UVA1 strongly increased VEGF secretion in a dose- and time-dependent manner, without significantly affecting ET-1 release. Irradiation of TGF-β1-stimulated fibroblasts resulted in a synergistic effect on increasing levels of VEGF but not ET-1 after 48 h. Cobalt chloride stimulated the secretion of VEGF by fibroblasts; the effects of TGF-β1 and cobalt were additive. However, no significant effect of cobalt chloride on ET-1 secretion was observed, suggesting that ET-1 production in fibroblasts is not oxygen-sensitive. The expression of NEP was not modified by TGF-β1 or UVA1 radiation. Addition of a neutralizing anti-CD10 antibody to fibroblast cultures downregulated CD10 expression at the cell surface without changing ET-1 levels in cell supernatants after 24 or 48 h. This suggests that membrane-bound NEP has minimal or no activity against secreted ET-1. Conclusions Taken together, these results underline the major role played by TGF-β1 in increasing VEGF secretion by fibroblasts. This, as well as the documented effect of UVA1 on increasing VEGF production, may have implications for wound healing in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2133.2000.03707.x
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  • 3
    Electronic Resource
    Electronic Resource
    In vitro reconstructed mucosa-integrating Langerhans' cells (2003)
    Oxford, UK : Munksgaard International Publishers
    Experimental dermatology 12 (2003), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  All three-dimensional in vitro mucosal models constructed, thus far, have only been reconstituted by epithelial cells. We have developed a reconstructed oral and vaginal epithelium that integrates Langerhans' cells (LC), the dendritic cells (DC) of malpighian epithelia. The epithelium was composed of gingival or vaginal keratinocytes seeded on a de-epidermized dermis (DED) and grown in submerged culture for 2 weeks. LC precursors, obtained after differentiation of cord blood-derived CD34+ hematopoietic progenitor cells (CD34+HPC) by granulocyte macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β) and Flt3-ligand (Flt3-L), were introduced after 6–8 days of culture into the reconstituted epithelium. The in vitro reconstituted mucosal epithelium formed a multilayered, well-differentiated epithelial structure, confirmed by the immunohistochemical expression of cytokeratins 4, 6, 10, 13, 14, 16 and involucrin. LC were identified in the basal and suprabasal epithelial layers by CD1a antigen, S100 protein and Langerin/CD207 expression, and by transmission electron microscopy. Type IV collagen was expressed at the chorio–epithelial junction, and most ultrastructural features of this junction were visualized by electron microscopy. This in vitro reconstructed gingiva or vagina integrating LC represents interesting models very similar to native tissues. Because LC play an important role in the mucosal immune system, our models could be useful for conducting studies on interactions with pathogenic agents (viruses, bacteria etc.), as well as in pharmacological, toxicological and clinical research.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2003.00108.x
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  • 4
    Electronic Resource
    Electronic Resource
    Withdrawal of TNF-α after the fifth day of differentiation of CD34+ cord blood progenitors generates a homogeneous population of Langerhans cells and delays their maturation (2003)
    Oxford, UK : Blackwell Science Ltd
    Experimental dermatology 12 (2003), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Human cord blood CD34+ progenitors cultured in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β) generate a heterogeneous population of dendritic cells (DC), including Langerhans cells (LC). This combination of cytokines has been shown to be crucial for differentiation into LC. After day 5 of culture, TNF-α has been maintained in the medium in most studies despite the observation of spontaneous maturation of LC after day 12. Five-day samples of in vitro differentiated LC were cultured in parallel with or without TNF-α. The absence of TNF-α was shown to: (1) slow down proliferation without triggering apoptotic cell death, (2) enhance the percentage of LC, (3) delay or abrogat the expression of CD83, CD86, HLA-DR and CD208 molecules, and (4) maintain endocytosis by receptor and macropinocytosis. The withdrawal of TNF-α abrogated the spontaneous synthesis of matrix metalloproteinases. At day 12, TNF-α-deprived LC were less efficient in allogeneic T cell activation than LC cultivated with TNF-α. These data indicate that the suppression of TNF-α after day 5 maintains cells in an immature state and provides a population with 80% of LC at day 12.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2003.00043.x
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  • 5
    Electronic Resource
    Electronic Resource
    IL-4 and interferon-γ differentially modulate vascular endothelial growth factor release from normal human keratinocytes and fibroblasts (2002)
    Oxford, UK : Munksgaard International Publishers
    Experimental dermatology 11 (2002), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: IL-4 and interferon-γ (IFN-γ) are crucial modulators of the immune system and are reported as active antitumor agents and potent inhibitors of angiogenesis. We investigated the effects of these two cytokines on the expression of vascular endothelial growth factor (VEGF), a mediator of major importance in the angiogenesis associated with inflammation, wound healing and tumor invasion and expressed by activated keratinocytes and dermal fibroblasts. Human keratinocytes (HK) and fibroblasts (HF) derived from foreskins, were further cultured during 24 h in defined medium, supplemented or not with the selected growth factors, EGF and TGF-β1, respectively, before receiving the addition of either IL-4 or IFN-γ during 24 and 48 h. In basal conditions, fibroblasts produced smaller amounts of VEGF than keratinocytes; the addition of growth factors to the skin cells induced a drastic increase of VEGF secretion. In HF, the basal level of VEGF secretion was reduced by IFN-γ and slightly increased by IL-4 whereas in HK, IFN-γ enhanced the secretion of VEGF after 48 h and IL-4 either tended to reduce VEGF secretion or did not exert any effect. Similar but more significant results were observed in skin cells activated by growth-stimulating factors. The association of IL-4 and IFN-γ mimicked the effects of IFN-γ alone both in HF and HK. Taken together, these results indicate opposite effects of IFN-γ and IL-4 on VEGF expression from normal and activated HF and HK. IL-4 may be considered as a poor modulator of VEGF secretion by dermal and epidermal cells. Conversely, IFN-γ appears as a prominent and versatile mediator in the desregulated angiogenesis associated with inflammatory skin reactions characterized by a T-helper type 1 cell-mediated response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2002.110305.x
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  • 6
    Electronic Resource
    Electronic Resource
    Modulation of endothelin-1 in normal human keratinocytes by UVA1/B radiations, prostaglandin E2 and peptidase inhibitors (2000)
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In the skin, keratinocytes synthesize and secrete endothelin-1 (ET-1), a potent vasoconstrictor peptide which acts also as a growth factor for most skin cells. The aim of the study was to test the effects of UVA1 and the associations UVA1/B on the expression of ET-1 in normal human keratinocytes and to determine whether exogenously added prostaglandin E2 (PGE2) regulated ET-1 expression. As ET-1 is susceptible to degradation, we also evaluated whether ET-1 secretion was modulated by peptidase inhibitors. Our results showed that UVA1 (365 nm) did not modify the levels of preproET-1 mRNA and protein. Moreover, the associations UVA1+UVB or UVB+UVA1 down-regulated the overexpression of secreted ET-1 induced by UVB alone. PGE2 at 10−5 M reduced the expression of ET-1 at the mRNA and protein levels but did not exert any significant modification at lower concentrations from 10−10 to 10−6 M. Phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, drastically decreased the amount of ET-1 accumulating in the culture medium in basal conditions or after UVB irradiation. Conversely, thiorphan, a specific inhibitor of neutral endopeptidase (NEP), rather increased the levels of ET-1 secretion mainly after UVB irradiation. Taken together, the results showed that normal human keratinocytes secrete and partly degrade ET-1 through ECE and NEP pathways and pointed out a differential regulation of ET-1 by UVB and UVA1 radiations without any noticeable role for PGE2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2000.009006401.x
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  • 7
    Electronic Resource
    Electronic Resource
    Comparative expression of vascular endothelial growth factor family members, VEGF-B, -C and -D, by normal human keratinocytes and fibroblasts (2004)
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Experimental dermatology 13 (2004), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  The vascular endothelial growth factor (VEGF) family includes the related polypeptides VEGF-B, -C and -D, which contribute to endothelial and lymphatic vessel development. The parental VEGF molecule, VEGF-A, has been widely described in the skin, but the other members of the VEGF family have not yet been reported.The aim of our study was to determine whether the two main skin cells, keratinocytes and fibroblasts, expressed VEGF-B, -C and -D in basal condition and after stimulation by either growth factors or the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α). Reverse-transcription polymerase chain reaction (RT-PCR) analysis on cultured normal human keratinocytes (NHKs) and normal human fibroblasts (NHFs) allowed the detection of different levels of VEGF-B, -C and -D mRNA, in both cell types with similar RT-PCR products in the skin cells. A semi-quantitative evaluation of the VEGF family proteins by dot blot, using the different human recombinant VEGFs, showed different levels of VEGF-B, -C and -D, in NHKs and NHFs. After cell stimulation by growth factors (epidermal growth factor (EGF) and transforming growth factor-β1 (TGF-β1) for NHKs and NHFs, respectively), a significant up-regulation of the VEGF family member proteins was observed in NHFs but not in NHKs. Conversely, TNF-α did not exert a significant effect. However, we could not detect any transcriptional modification in stimulated cells, whatever the stimulation duration. The addition of cycloheximide to the cell cultures strongly inhibited the increase of VEGF proteins in TGF-β1-stimulated NHFs. Taken together, the results underline the major role played by NHFs in the elaboration of the VEGF family proteins known to regulate wound healing, chronic inflammation and tumour angiogenesis and lymphangiogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2004.00137.x
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  • 8
    Electronic Resource
    Electronic Resource
    Calcium triggers β-defensin (hBD-2 and hBD-3) and chemokine macrophage inflammatory protein-3α (MIP-3α/CCL20) expression in monolayers of activated human keratinocytes (2003)
    Oxford, UK : Munksgaard International Publishers
    Experimental dermatology 12 (2003), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  The inducible epidermal β-defensins and the chemokine macrophage inflammatory protein-3α (MIP-3α/CCL20) are important mediators involved in innate and adaptive immunity and in the recruitment of immune cells. The aim of our study was to determine whether calcium could trigger the induction of β-defensins (hBD-2 and hBD-3) mRNA and the release of MIP-3α by normal human keratinocyte monolayers. Epidermal cells derived from foreskin were cultured in defined medium supplemented with different calcium levels (0.09, 0.8 and 1.7 mM) and were stimulated or not with the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α 1–500 ng/ml) or interferon-γ (IFN-γ 1–100 ng/ml). A high calcium concentration (1.7 mM) alone applied in culture medium for 4 days was sufficient to induce hBD-2 and hBD-3 mRNA expression. Whatever interindividual variability in the expression of hBD-2 and hBD-3 mRNA and MIP-3α secretion, the addition of TNF-α for a short duration (16 h), initiated a dose-dependent and coordinated up-regulation of hBD2 mRNA and MIP-3α release in keratinocyte cultures. Unlike hBD-2, hBD-3 mRNA was preferentially stimulated by IFN-γ rather than TNF-α. In our experimental conditions, l-isoleucine, described to stimulate β-defensins in bovine epithelial cells, did not exert any effect either on hBD-2 and hBD-3 transcripts or MIP-3α protein. Taken together, these results confirm the major role of the maturation/differentiation process of normal human keratinocytes in the induction of inducible β-defensins and MIP-3α chemokine, which contribute in vivo to the immunosurveillance of the skin barrier function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2003.00086.x
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  • 9
    Electronic Resource
    Electronic Resource
    Evidence for modulation of human epidermal differentiation and remodelling by CD40 (2003)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 148 (2003), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background It is widely accepted that CD40 plays a critical role in the regulation of immune response. However, the significance of CD40 expression on normal human keratinocytes is only partially known. Objectives To perform a morphological re-examination of the role of CD40 on the differentiation of human keratinocytes and remodelling of the epidermis. Methods Keratinocytes were grown on fibroblasts transfected with the CD40 ligand (CD40L) to investigate the formation of epidermal sheets in culture under the influence of the CD40L. Control experiments were carried out using the same cells but transfected with CD32. Further, three specific anti-CD40 monoclonal antibodies were used as soluble agonists to analyse the effect of CD40 ligation on keratinocyte differentiation. Results Epidermal sheets developing from keratinocytes cocultured with fibroblasts transfected with CD40L but not with CD32 showed an up to 50% reduction in thickness compared with control sheets. This change depended mostly on cellular flattening and a decrease in the number of cell layers, and was coincident with a transient decrease in cell surface CD40 immunoreactivity. On the other hand, normal epidermis, and freshly isolated and cultured keratinocytes revealed a predominant CD40+/Ki-67– phenotype that was demonstrated by double immunocytochemistry. Consistent with these observations, keratinocytes primed with interferon-γ responded to the three soluble agonists, but not to control IgG1, producing immunoreactive (pro)filaggrin and displaying morphological changes in shape and size equivalent to those seen in differentiated cells. Conclusions As a whole, our findings provide evidence that CD40+ keratinocytes represent a poorly differentiated population, not actively engaged in the cell cycle, which under specific stimulation is committed towards terminal differentiation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2003.05300.x
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  • 10
    Electronic Resource
    Electronic Resource
    Modulation of substance P and somatostatin receptors in cutaneous lymphocytic inflammatory and tumoral infiltrates (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of the European Academy of Dermatology and Venereology 15 (2001), S. 0 
    Details
    ISSN: 1468-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The expression of receptors for neuropeptides in the skin is modified in skin diseases.〈section xml:id="abs1-3"〉〈title type="main"〉ObjectiveWe studied the cutaneous expression of substance P (SP) and somatostatin (SOM) receptors (SPR and SSTR, respectively) in skin affected by cutaneous inflammatory or tumoral T-cell infiltrates because these two neuropeptides are the ones most involved in inflammation.〈section xml:id="abs1-4"〉〈title type="main"〉MethodsWe revealed expression of these receptors using a binding in situ technique that gave highly specific results. Skin biopsies were incubated with biotinylated neuropeptides (SP or SOM).〈section xml:id="abs1-5"〉〈title type="main"〉ResultsIn normal skin, SSTR were observed on blood vessels, smooth muscle fibres and sweat glands. SSTR expression was modified only when expressed by keratinocytes in Ofuji papuloerythroderma and by plasmocytes in plasmocytoma. SPR distribution was not modified in subjects with atopic dermatitis or lupus. The expression of SPR in the epidermis was diminished in Ofuji papuloerythroderma and parapsoriasis and absent in mycosis fungoides.〈section xml:id="abs1-6"〉〈title type="main"〉ConclusionsThese results suggest that malignant lymphocytic infiltrates can inhibit SPR expression on keratinocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1468-3083.2001.00259.x
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