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  • Werner, Sabine  (46)
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  • 1
    Language: English
    In: Cell cycle (Georgetown, Tex.), 01 August 2010, Vol.9(15), pp.2917-8
    Description: Comment on: Schäfer M, et al. Genes Dev 2010; 24:1045-58.
    Keywords: Ultraviolet Rays ; Epidermis -- Metabolism ; Nf-E2-Related Factor 2 -- Metabolism ; Protective Agents -- Metabolism
    ISSN: 15384101
    E-ISSN: 1551-4005
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  • 2
    Language: English
    In: Journal of Investigative Dermatology, July 2011, Vol.131(7), pp.1409-1411
    Description: Human skin serves as a barrier against multiple environmental insults, including pathogenic microorganisms, pollutants, toxic chemicals, and UV radiation. In the outermost layer of the epidermis, the cornified envelope functions as a mechanical and permeability barrier. In this issue, Vermeij report a novel function of cornified envelope proteins as a first-line antioxidant barrier to protect the body from damage induced by reactive oxygen species.
    Keywords: Medicine
    ISSN: 0022-202X
    E-ISSN: 1523-1747
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  • 3
    Language: English
    In: The Journal of clinical investigation, November 2012, Vol.122(11), pp.3965-76
    Description: Psoriasis is a chronic inflammatory disorder of the skin affecting approximately 2% of the world's population. Accumulating evidence has revealed that the IL-23/IL-17/IL-22 pathway is key for development of skin immunopathology. However, the role of keratinocytes and their crosstalk with immune cells at the onset of disease remains poorly understood. Here, we show that IL-36R-deficient (Il36r-/-) mice were protected from imiquimod-induced expansion of dermal IL-17-producing γδ T cells and psoriasiform dermatitis. Furthermore, IL-36R antagonist-deficient (Il36rn-/-) mice showed exacerbated pathology. TLR7 ligation on DCs induced IL-36-mediated crosstalk with keratinocytes and dermal mesenchymal cells that was crucial for control of the pathological IL-23/IL-17/IL-22 axis and disease development. Notably, mice lacking IL-23, IL-17, or IL-22 were less well protected from disease compared with Il36r-/- mice, indicating an additional distinct activity of IL-36 beyond induction of the pathological IL-23 axis. Moreover, while the absence of IL-1R1 prevented neutrophil infiltration, it did not protect from acanthosis and hyperkeratosis, demonstrating that neutrophils are dispensable for disease manifestation. These results highlight a central and unique IL-1-independent role for IL-36 in control of the IL-23/IL-17/IL-22 pathway and development of psoriasiform dermatitis.
    Keywords: Cell Communication -- Immunology ; Dendritic Cells -- Immunology ; Dermatitis -- Immunology ; Interleukin-1 -- Immunology ; Keratinocytes -- Immunology ; Psoriasis -- Immunology
    ISSN: 00219738
    E-ISSN: 1558-8238
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  • 4
    Language: English
    In: Free Radical Biology and Medicine, November 2015, Vol.88, pp.243-252
    Description: The skin is frequently exposed to environmental challenges, such as UV irradiation, toxic chemicals, and mechanical wounding. These insults cause an increase in the levels of reactive oxygen species, resulting in oxidative stress and concomitant inflammation, skin aging, and even cancer development. Therefore, an efficient antioxidant defense strategy is of major importance in this tissue. Since the Nrf2 transcription factor regulates a battery of genes involved in the defense against reactive oxygen species and in compound metabolism, it plays a key role in skin homeostasis, repair, and disease. In this review we summarize current knowledge on the expression and function of Nrf2 in normal skin and its role in the acute and chronic UV response as well as in the pathogenesis of epithelial skin cancer and of different inflammatory skin diseases. Finally, we discuss the potential of Nrf2-activating compounds for skin protection under stress conditions and for the treatment of major human skin disorders.
    Keywords: Nrf2 ; Oxidative Stress ; Skin Cancer ; Wound Healing ; Inflammation ; Chemoprevention ; Biology ; Anatomy & Physiology
    ISSN: 0891-5849
    E-ISSN: 1873-4596
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  • 5
    Language: English
    In: PLoS ONE, 01 January 2013, Vol.8(2), p.e56625
    Description: The nuclear factor erythroid 2-related factor 2 (Nrf2) governs the expression of antioxidant and phase II detoxifying enzymes. Nrf2 activation can prevent or reduce cellular damage associated with several types of injury in many different tissues and organs. Dominant mutations in Cu/Zn-superoxide dismutase (SOD1) cause familial forms of amyotrophic lateral sclerosis (ALS), a fatal disorder characterized by the progressive loss of motor neurons and subsequent muscular atrophy. We have previously shown that Nrf2 activation in astrocytes delays neurodegeneration in ALS mouse models. To further investigate the role of Nrf2 in ALS we determined the effect of absence of Nrf2 or its restricted overexpression in neurons or type II skeletal muscle fibers on symptoms onset and survival in mutant hSOD1 expressing mice. We did not observe any detrimental effect associated with the lack of Nrf2 in two different mutant hSOD1 animal models of ALS. However, restricted Nrf2 overexpression in neurons or type II skeletal muscle fibers delayed disease onset but failed to extend survival in hSOD1(G93A) mice. These results highlight the concept that not only the pharmacological target but also the cell type targeted may be relevant when considering a Nrf2-mediated therapeutic approach for ALS.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 6
    In: PLoS ONE, 2013, Vol.8(4)
    Description: The nuclear factor erythroid 2-related factor 2 (Nrf2) governs the expression of antioxidant and phase II detoxifying enzymes. Nrf2 activation can prevent or reduce cellular damage associated with several types of injury in many different tissues and organs. Dominant mutations in Cu/Zn-superoxide dismutase (SOD1) cause familial forms of amyotrophic lateral sclerosis (ALS), a fatal disorder characterized by the progressive loss of motor neurons and subsequent muscular atrophy. We have previously shown that Nrf2 activation in astrocytes delays neurodegeneration in ALS mouse models. To further investigate the role of Nrf2 in ALS we determined the effect of absence of Nrf2 or its restricted overexpression in neurons or type II skeletal muscle fibers on symptoms onset and survival in mutant hSOD1 expressing mice. We did not observe any detrimental effect associated with the lack of Nrf2 in two different mutant hSOD1 animal models of ALS. However, restricted Nrf2 overexpression in neurons or type II skeletal muscle fibers delayed disease onset but failed to extend survival in hSOD1G93A mice. These results highlight the concept that not only the pharmacological target but also the cell type targeted may be relevant when considering a Nrf2-mediated therapeutic approach for ALS.
    Keywords: Correction
    E-ISSN: 1932-6203
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  • 7
    Language: English
    In: Oncoscience, 2014, Vol.1(6), pp.392-3
    Keywords: Editorial;
    ISSN: 2331-4737
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  • 8
    Language: English
    In: Seminars in Immunology, August 2014, Vol.26(4), pp.321-328
    Description: The attraction and activation of immune cells is an important response of the skin to injury and allows an efficient defense against invading pathogens. In addition, immune cells fulfill various functions that are important for the repair process. An exaggerated inflammatory response, however, is a hallmark of chronic, non-healing wounds. Therefore, it is essential to strictly control and coordinate the levels and activities of various immune cells in normal and wounded skin. Recent studies provided insight into the molecular mechanisms underlying the inflammatory response after wounding, and various transcriptional regulators involved in this process have been identified. This review summarizes our current knowledge on the function of different transcription factors in wound repair, with particular emphasis on proteins with a documented role in the control of wound inflammation.
    Keywords: Granulation Tissue ; Inflammation ; Transcription Factor ; Scar ; Medicine ; Biology
    ISSN: 1044-5323
    E-ISSN: 1096-3618
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  • 9
    Language: English
    In: Journal of Crohn's & colitis, 01 April 2017, Vol.11(4), pp.485-499
    Description: The transcription factor Nrf2 is a major modulator of the cellular antioxidant response. Oxidative burst of infiltrating macrophages leads to a massive production of reactive oxygen species in inflamed tissue of inflammatory bowel disease patients. This oxidative burst contributes to tissue destruction and epithelial permeability, but it is also an essential part of the antibacterial defence. We therefore investigated the impact of the Nrf2 orchestrated antioxidant response in both acute and chronic intestinal inflammation. To study the role of Nrf2 overexpression in mucosal inflammation, we used transgenic mice conditionally expressing a constitutively active form of Nrf2 [caNrf2] either in epithelial cells or in the myeloid cell lineage. Acute colitis was induced by dextran sulphate sodium [DSS] in transgenic and control animals, and changes in gene expression were evaluated by genome-wide expression studies. Long-term effects of Nrf2 activation were studied in mice with an IL-10-/- background. Expression of caNrf2 either in epithelial cells or myeloid cells resulted in aggravation of DSS-induced acute colitis. Aggravation of inflammation by caNrf2 was not observed in the IL-10-/- model of spontaneous chronic colitis, where even a trend towards reduced prolapse rate was observed. Our findings show that a well-balanced redox homeostasis is as important in epithelial cells as in myeloid cells during induction of colitis. Aggravation of acute DSS colitis in response to constitutive Nrf2 expression emphasises the importance of tight regulation of Nrf2 during the onset of intestinal inflammation.
    Keywords: Colitis ; Nrf2 ; Reactive Oxygen Species ; Colitis -- Etiology ; Nf-E2-Related Factor 2 -- Physiology
    ISSN: 18739946
    E-ISSN: 1876-4479
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  • 10
    Language: English
    In: Nat Commun, 2018, Vol.9(1), pp.236-236
    Description: Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-β signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.
    Keywords: Article;
    ISSN: 2041-1723
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