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Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice
Afadin is a filamentous actin-binding protein and a mediator of nectin signaling. Nectins are Ig-like cell adhesion molecules, and the nectin family is composed of four members, nectin-1 to nectin-4. Nectins show homophilic and heterophilic interactions with other nectins or proteins on adjacent cel...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BlackWell Publishing Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231224/ https://www.ncbi.nlm.nih.gov/pubmed/25297509 http://dx.doi.org/10.1111/gtc.12184 |
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author | Yoshida, Toshiyuki Iwata, Takanori Takai, Yoshimi Birchmeier, Walter Yamato, Masayuki Okano, Teruo |
author_facet | Yoshida, Toshiyuki Iwata, Takanori Takai, Yoshimi Birchmeier, Walter Yamato, Masayuki Okano, Teruo |
author_sort | Yoshida, Toshiyuki |
collection | PubMed |
description | Afadin is a filamentous actin-binding protein and a mediator of nectin signaling. Nectins are Ig-like cell adhesion molecules, and the nectin family is composed of four members, nectin-1 to nectin-4. Nectins show homophilic and heterophilic interactions with other nectins or proteins on adjacent cells. Nectin signaling induces formation of cell–cell junctions and is required for the development of epithelial tissues, including skin. This study investigated the role of afadin in epithelial tissue development and established epithelium-specific afadin-deficient (CKO) mice. Although showing no obvious abnormality in the skin development and homeostasis, the mice showed the reduced neutrophil infiltration into the epidermis during chemical-induced inflammation with 12-O-tetradecanoylphorbol 13-acetate (TPA). Immunohistochemical and quantitative real-time PCR analyses showed that the expression levels of cytokines including Cxcl2, Il-1β and Tnf-α were reduced in CKO keratinocytes compared with control keratinocytes during TPA-induced inflammation. Primary-cultured skin keratinocytes from CKO mice also showed reduced expression of these cytokines and weak activation of Rap1 compared with those from control mice after the TPA treatment. These results suggested a remarkable function of afadin, which was able to enhance cytokine expression through Rap1 activation in keratinocytes during inflammation. |
format | Online Article Text |
id | pubmed-4231224 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BlackWell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-42312242014-12-15 Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice Yoshida, Toshiyuki Iwata, Takanori Takai, Yoshimi Birchmeier, Walter Yamato, Masayuki Okano, Teruo Genes Cells Original Articles Afadin is a filamentous actin-binding protein and a mediator of nectin signaling. Nectins are Ig-like cell adhesion molecules, and the nectin family is composed of four members, nectin-1 to nectin-4. Nectins show homophilic and heterophilic interactions with other nectins or proteins on adjacent cells. Nectin signaling induces formation of cell–cell junctions and is required for the development of epithelial tissues, including skin. This study investigated the role of afadin in epithelial tissue development and established epithelium-specific afadin-deficient (CKO) mice. Although showing no obvious abnormality in the skin development and homeostasis, the mice showed the reduced neutrophil infiltration into the epidermis during chemical-induced inflammation with 12-O-tetradecanoylphorbol 13-acetate (TPA). Immunohistochemical and quantitative real-time PCR analyses showed that the expression levels of cytokines including Cxcl2, Il-1β and Tnf-α were reduced in CKO keratinocytes compared with control keratinocytes during TPA-induced inflammation. Primary-cultured skin keratinocytes from CKO mice also showed reduced expression of these cytokines and weak activation of Rap1 compared with those from control mice after the TPA treatment. These results suggested a remarkable function of afadin, which was able to enhance cytokine expression through Rap1 activation in keratinocytes during inflammation. BlackWell Publishing Ltd 2014-11 2014-10-09 /pmc/articles/PMC4231224/ /pubmed/25297509 http://dx.doi.org/10.1111/gtc.12184 Text en © 2014 The Authors. Genes to Cells published by Wiley Publishing Asia Pty Ltd and the Molecular Biology Society of Japan. http://creativecommons.org/licenses/by/3.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Yoshida, Toshiyuki Iwata, Takanori Takai, Yoshimi Birchmeier, Walter Yamato, Masayuki Okano, Teruo Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title | Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title_full | Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title_fullStr | Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title_full_unstemmed | Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title_short | Afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
title_sort | afadin requirement for cytokine expressions in keratinocytes during chemically induced inflammation in mice |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231224/ https://www.ncbi.nlm.nih.gov/pubmed/25297509 http://dx.doi.org/10.1111/gtc.12184 |
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