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      Skin renewal activity of non-thermal plasma through the activation of β-catenin in keratinocytes

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          Abstract

          For recent years, devices that generate non-thermal plasma (NTP) have been introduced into the field of dermatology. Since NTP has demonstrated strong anti-pathogenic activity with safety of use, NTP was first applied to sterilize the skin surface to aid in the healing of various kinds of skin diseases. However, the effect of NTP on skin regeneration has not yet been fully explored. In this study, the effect of NTP on the growth of keratinocytes was tested using the HaCaT human keratinocyte cell line and HRM2 hairless mice. Treatment with NTP allowed confluent keratinocytes to escape from G1 cell cycle arrest and increased the proportion of cells in S and G2 phases. In particular, NTP treatment immediately dispersed E-cadherin-mediated cell-to-cell interactions, resulting in the translocation of β-catenin to the nucleus and leading to the enhanced transcription of target genes including c-MYC and cyclin D1. Moreover, repeated treatment of the mice with NTP also stimulated epidermal expansion by activating β-catenin in the epidermal cells. The symptoms of cellular DNA damage were not detected after NTP treatment. Taken together, these results demonstrate that NTP may be employed as a new type of skin regenerating device.

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          The cell-cell adhesion molecule E-cadherin.

          This review is dedicated to E-cadherin, a calcium-dependent cell-cell adhesion molecule with pivotal roles in epithelial cell behavior, tissue formation, and suppression of cancer. As founder member of the cadherin superfamily, it has been extensively investigated. We summarize the structure and regulation of the E-cadherin gene and transcript. Models for E-cadherin-catenin complexes and cell junctions are presented. The structure of the E-cadherin protein is discussed in view of the diverse functions of this remarkable protein. Homophilic and heterophilic adhesion are compared, including the role of E-cadherin as a receptor for pathogens. The complex post-translational processing of E-cadherin is reviewed, as well as the many signaling activities. The role of E-cadherin in embryonic development and morphogenesis is discussed for several animal models. Finally, we review the multiple mechanisms that disrupt E-cadherin function in cancer: inactivating somatic and germline mutations, epigenetic silencing by DNA methylation and epithelial to mesenchymal transition-inducing transcription factors, and dysregulated protein processing.
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            Epidermal homeostasis: a balancing act of stem cells in the skin.

            The skin epidermis and its array of appendages undergo ongoing renewal by a process called homeostasis. Stem cells in the epidermis have a crucial role in maintaining tissue homeostasis by providing new cells to replace those that are constantly lost during tissue turnover or following injury. Different resident skin stem cell pools contribute to the maintenance and repair of the various epidermal tissues of the skin, including interfollicular epidermis, hair follicles and sebaceous glands. Interestingly, the basic mechanisms and signalling pathways that orchestrate epithelial morphogenesis in the skin are reused during adult life to regulate skin homeostasis.
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              Deconstructing the skin: cytoarchitectural determinants of epidermal morphogenesis.

              To provide a stable environmental barrier, the epidermis requires an integrated network of cytoskeletal elements and cellular junctions. Nevertheless, the epidermis ranks among the body's most dynamic tissues, continually regenerating itself and responding to cutaneous insults. As keratinocytes journey from the basal compartment towards the cornified layers, they completely reorganize their adhesive junctions and cytoskeleton. These architectural components are more than just rivets and scaffolds - they are active participants in epidermal morphogenesis that regulate epidermal polarization, signalling and barrier formation.
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                Author and article information

                Contributors
                jwhong@pusan.ac.kr
                ki91000m@pusan.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                21 July 2017
                21 July 2017
                2017
                : 7
                : 6146
                Affiliations
                [1 ]ISNI 0000 0001 0719 8572, GRID grid.262229.f, Department of Internal Medicine, School of Korean Medicine, , Pusan National University, ; Yangsan, South Korea
                [2 ]ISNI 0000 0001 0719 8572, GRID grid.262229.f, Department of Oral Anatomy and Cell Biology, School of Dentistry, , Pusan National University, ; Yangsan, South Korea
                [3 ]ISNI 0000 0004 0470 5454, GRID grid.15444.30, Department of Biochemistry, College of Life Science and Biotechnology, , Yonsei University, ; Seoul, South Korea
                [4 ]ISNI 0000 0001 0719 8572, GRID grid.262229.f, Department of Electrical Engineering, , Pusan National University, ; Busan, South Korea
                [5 ]ISNI 0000 0000 8611 7824, GRID grid.412588.2, (Bio)medical Research Institute, , Pusan National University Hospital, ; Yangsan, South Korea
                Article
                6661
                10.1038/s41598-017-06661-7
                5522407
                28733577
                acd64139-8994-47bd-a08c-7e7a23bb07e9
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 20 February 2017
                : 15 June 2017
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