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Berlin Brandenburg

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  • 1
    Language: English
    In: PLoS ONE, 01 January 2018, Vol.13(9), p.e0204318
    Description: BACKGROUND AND OBJECTIVES:Microneedling therapy is a widely used technique in dermatology. However, little is known about the underlying molecular effects of this therapy on extracellular matrix remodeling, wound healing, and inflammation. The aim of this study was to examine morphological...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 2
    Language: English
    In: PLoS ONE, 01 January 2016, Vol.11(1), p.e0146325
    Description: INTRODUCTION:Interferon alpha (IFNα) is routinely used in the clinical practice for adjuvant systemic melanoma therapy. Understanding the molecular mechanism of IFNα effects and prediction of response in the IFNα therapy regime allows initiation and continuation of IFNα treatment for responder...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: The Journal of Allergy and Clinical Immunology, February 2012, Vol.129(2), pp.426-433.e8
    Description: Atopic dermatitis (AD) is an inflammatory skin disease affecting 10% to 20% of children and 1% to 3% of adults in industrialized countries. Enhanced expression of IL-31 is detected in skin samples of patients with AD, but its physiological relevance is not known. We sought to determine the role of IL-31 in skin differentiation. We used human 3-dimensional organotypic skin models with either primary keratinocytes or HaCaT keratinocytes with inducible IL-31 receptor α to evaluate the effect of IL-31. The consequences were studied by using histology, the expression of markers analyzed by immunofluoresence and quantitative RT-PCR, and gene expression arrays. We observed that IL-31 interferes with keratinocyte differentiation. Gene expression analysis revealed a limited set of genes deregulated in response to IL-31, including and . In HaCaT keratinocytes with inducible IL-31 receptor α, IL-31 inhibited proliferation upon induction of IL-31 receptor α by inducing cell cycle arrest. As in primary cells, IL-31–treated HaCaT cells elicited a differentiation defect in organotypic skin models, associated with reduced epidermal thickness, disturbed epidermal constitution, altered alignment of the stratum basale, and poor development of the stratum granulosum. The differentiation defect was associated with a profound repression of terminal differentiation markers, including filaggrin, an essential factor for skin barrier formation, and a reduced lipid envelope. The highly induced proinflammatory cytokines IL-20 and IL-24 were responsible for part of the effect on expression and thus for terminal differentiation. Our study suggests that IL-31 is an important regulator of keratinocyte differentiation and demonstrates a link between the presence of IL-31 in skin, as found in patients with AD, and filaggrin expression.
    Keywords: Atopic Dermatitis ; Differentiation ; Filaggrin ; Hacat ; Il-20 ; Il-24 ; Il-31 ; Keratinocyte ; Organotypic Skin Model ; Proliferation ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 4
    Language: English
    In: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, February 2017, Vol.31(2), pp.526-543
    Description: The response of the skin to harmful environmental agents is shaped decisively by the status of the immune system. Keratinocytes constitutively express and secrete the chemokine-like mediator, macrophage migration inhibitory factor (MIF), more strongly than dermal fibroblasts, thereby creating a MIF gradient in skin. By using global and epidermis-restricted Mif-knockout (Mif and K14-Cre; Mif) mice, we found that MIF both recruits and maintains antigen-presenting cells in the dermis/epidermis. The reduced presence of antigen-presenting cells in the absence of MIF was associated with accelerated and increased formation of nonmelanoma skin tumors during chemical carcinogenesis. Our results demonstrate that MIF is essential for maintaining innate immunity in skin. Loss of keratinocyte-derived MIF leads to a loss of control of epithelial skin tumor formation in chemical skin carcinogenesis, which highlights an unexpected tumor-suppressive activity of MIF in murine skin.-Brocks, T., Fedorchenko, O., Schliermann, N., Stein, A., Moll, U. M., Seegobin, S., Dewor, M., Hallek, M., Marquardt, Y., Fietkau, K., Heise, R., Huth, S., Pfister, H., Bernhagen, J., Bucala, R., Baron, J. M., Fingerle-Rowson, G. Macrophage migration inhibitory factor protects from nonmelanoma epidermal tumors by regulating the number of antigen-presenting cells in skin.
    Keywords: Cd44 ; Cd74 ; Dmba/Tpa ; Chemokine ; Skin Carcinogenesis ; Macrophage Migration-Inhibitory Factors -- Metabolism ; Skin -- Cytology ; Skin Neoplasms -- Chemically Induced
    ISSN: 08926638
    E-ISSN: 1530-6860
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  • 5
    Language: English
    In: Experimental dermatology, May 2011, Vol.20(5), pp.450-2
    Description: Several transport proteins are constitutively expressed in skin cells, but the putative role of the ABC transporter P-glycoprotein (P-gp) in human skin is yet unknown. Therefore, we analysed mRNA and protein expression and localization of P-gp in human skin. Using qRT-PCR, we demonstrated a strong MDR1 mRNA expression in whole skin specimens and dermis, whereas the expression of MDR1 in epidermis, epidermal keratinocytes or dermal fibroblasts was only weak. Immunohistochemistry confirmed mRNA data and revealed a marked expression of P-gp within sweat ducts, vessels, nerve sheaths and muscles of human skin and a moderate expression in basal epidermis. Our findings closely correlate with previous studies in murine skin supporting the role of P-gp in the uptake of compounds from the epidermal compartment and their secretion into the bloodstream and sweat ducts. It may also prevent the uptake of xenobiotics into the skin by functioning as a barrier located in the dermal vasculature.
    Keywords: ATP Binding Cassette Transporter, Subfamily B, Member 1 -- Genetics ; Dermis -- Metabolism ; Gene Expression -- Genetics ; Skin -- Metabolism
    ISSN: 09066705
    E-ISSN: 1600-0625
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  • 6
    Language: English
    In: Sci Rep, 2017, Vol.7(1), pp.15631-15631
    Description: Psoriasis is a T17-driven inflammatory disease affecting a significant proportion of the world population. The molecular consequences of IL-17 signaling in the skin are only partially understood. Therefore, we evaluated the IL-17A effects on organotypic 3-dimensional skin models and observed that IL-17A interfered with keratinocyte differentiation. In agreement with this phenotype, IL-17A repressed the expression of many genes encoding structural proteins. Moreover, genes encoding anti-microbial peptides were induced, resulting in a strengthening of the chemical barrier. Finally, we observed enhanced expression of the three IL-36 cytokines IL-36α, β and γ. We found that IL-36γ was secreted from keratinocytes in an inactive form and that neutrophilic proteases, including elastase, were capable of activating this cytokine. Functionally and similar to IL-17A, truncated IL-36 cytokines interfered with keratinocyte differentiation in 3D models. The molecular analysis revealed strong cooperative effects of IL-17A and IL-36 cytokines in regulating target genes, which was dependent on the proteolytic activation of the latter. Together these findings suggest an amplification cycle that can be initiated by IL-17A, involving IL-36 cytokines and immune cell derived proteases and resulting in active IL-36 cytokines which synergize with IL-17A. This amplification cycle might be relevant for a persistent psoriatic phenotype.
    Keywords: Article;
    ISSN: 2045-2322
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  • 7
    Language: English
    In: Archives of biochemistry and biophysics, 2011, Vol.508(2), pp.212-216
    Description: The multidrug resistance related proteins (MRPs) function as efflux transporters of a variety of large organic anions or their conjugates. In recent studies we demonstrated that antigen-presenting cells express a specific pattern of MRPs. MRP-mediated efflux activity of human monocyte-derived dendritic cells (moDCs) was analyzed using an in vitro transport assay. The efflux transport of radiolabeled contact allergens was inhibited using the specific MRP inhibitor indomethacin. Treatment with indomethacin increased intracellular concentration of [³H] eugenol and [³H] isoeugenol in moDCs. In addition by using MRP1 expressing inside-out membrane vesicles we revealed that the transport of eugenol is mediated by MRP1. Human DCs were employed to assess the sensitizing potential of contact allergens and alters their cytokine gene expression profile. Hence, to survey the functionality of indomethacin after stimulation with contact allergens IL-8 and TRIM16 regulation was measured by a DC-based in vitro assay. Incubation with isoeugenol after pre-treatment with indomethacin leads to increased IL-8 and TRIM16 gene expression. These results strongly support the functional role of MRPs in the active efflux of contact allergens also in antigen-presenting cells like moDCs, a novel mechanism which could possibly play a role in the pathogenesis of contact allergy. ; p. 212-216.
    Keywords: Anions ; Indomethacin ; In Vitro Studies ; Dendritic Cells ; Pathogenesis ; Tritium ; Active Transport ; Humans ; Radiolabeling ; Interleukin-8 ; Hypersensitivity ; Pretreatment ; Transporters ; Multiple Drug Resistance ; Allergens ; Eugenol ; Gene Expression
    ISSN: 0003-9861
    Source: AGRIS (Food and Agriculture Organization of the United Nations)
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  • 8
    Language: English
    In: Tissue Engineering Part A, 08/26/2014, p.140826231607006
    Description: Organotypic full-thickness skin-grafts (OTSG) are already an important technology for treating various skin conditions and are well-established for skin research and development. These obvious benefits are often impaired by the need of laborious production, their non-complete autologous composition and most importantly their lack of included vasculature. Therefore our study focused on combining a pre-vascularized dermal layer with an epidermis to cultivate full-thickness skin grafts incorporating capillary-like networks. It has been shown that pre-vascularization accelerates ingrowth of tissue-engineered grafts and it is a prerequisite to circumvent diffusion limits due to graft thickness. To obtain such a graft, we chose a dermal layer incorporating human umbilical vein endothelial cells (HuVEC) amidst human dermal fibroblasts (hdF) within a fibrin-based scaffold, seeded apically with human foreskin keratinocytes (hfKC). Our research investigated the used concept’s feasibility, as well as the effect of hfKC addition on the development of a well-connected capillary-like network after up to 21 days. Additionally, we evaluated the utilization of a custom-made constant flow bioreactor for simplified cultivation of these grafts, therefore possibly easing graft production and presumably increasing their cost-effectiveness. Skin grafts were assessed by conventional 2D-histology. Additionally software-assisted 3D evaluation of the capillary-like structure networks was performed by two-photon laser scanning microscopy (TPLSM) and subsequent image processing with ImagePro® Analyzer 7.0 software, hereby evaluating its platform technology power in the field of pre-vascularized skin grafts. All samples showed a capillary-like structure network, but we could report a significant reduction of its total length after 14 days of tri-culture with 5x105/cm² seeded hfKC, possibly indicating nutritional deficiencies for this particular high cell density experimental setup. Lower concentrations of hfKC did not affect the formation of the capillary-like structures significantly. The developed bioreactor simplified cultivation of pre-vascularized OTSC. However, a flow dependent reduction of capillary-like structures in 1 and 5 ml/min flow conditions occurred. We conclude that our technique for creating pre-vascularized OTSC is feasible. Additionally TPLSM is well suited for analyzing the pre-vascularization process. We hypothesize the handling benefits of our bioreactor can be preserved by using considerably lower flow rates while not impairing the forming of capillary-like structure networks.
    Keywords: Engineering;
    ISSN: 1937-3341
    E-ISSN: 1937-335X
    Source: Mary Ann Liebert (via CrossRef)
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  • 9
  • 10
    Language: English
    In: Archives of Biochemistry and Biophysics, 2011, Vol.508(2), pp.212-216
    Description: ► Indomethacin increased intracellular concentration of contact allergens in moDCs. ► Transport of eugenol is mediated by MRP-1. ► Indomethacin-and isoeugenol-dependent increase of IL-8 and TRIM16 expression. The multidrug resistance related proteins (MRPs) function as efflux transporters of a variety of large organic anions or their conjugates. In recent studies we demonstrated that antigen-presenting cells express a specific pattern of MRPs. MRP-mediated efflux activity of human monocyte-derived dendritic cells (moDCs) was analyzed using an transport assay. The efflux transport of radiolabeled contact allergens was inhibited using the specific MRP inhibitor indomethacin. Treatment with indomethacin increased intracellular concentration of [ H] eugenol and [ H] isoeugenol in moDCs. In addition by using MRP1 expressing inside-out membrane vesicles we revealed that the transport of eugenol is mediated by MRP1. Human DCs were employed to assess the sensitizing potential of contact allergens and alters their cytokine gene expression profile. Hence, to survey the functionality of indomethacin after stimulation with contact allergens IL-8 and TRIM16 regulation was measured by a DC-based assay. Incubation with isoeugenol after pre-treatment with indomethacin leads to increased IL-8 and TRIM16 gene expression. These results strongly support the functional role of MRPs in the active efflux of contact allergens also in antigen-presenting cells like moDCs, a novel mechanism which could possibly play a role in the pathogenesis of contact allergy.
    Keywords: Contact Allergens ; Dendritic Cell ; Multidrug Resistance Related Protein ; Transport ; Biology ; Chemistry ; Anatomy & Physiology
    ISSN: 0003-9861
    E-ISSN: 1096-0384
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