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Plasma gelsolin promotes re-epithelialization
Woundhealing disorders characterized by impaired or delayed re-epithelialization are a serious medical problem that is painful and difficult to treat. Gelsolin (GSN), a known actin modulator, supports epithelial cell regeneration and apoptosis. The aim of this study was to estimate the potential of...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120956/ https://www.ncbi.nlm.nih.gov/pubmed/30177722 http://dx.doi.org/10.1038/s41598-018-31441-2 |
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author | Wittmann, J. Dieckow, J. Schröder, H. Hampel, U. Garreis, F. Jacobi, C. Milczarek, A. Hsieh, K. L. Pulli, B. Chen, J. W. Hoogeboom, S. Bräuer, L. Paulsen, F. P. Schob, S. Schicht, M. |
author_facet | Wittmann, J. Dieckow, J. Schröder, H. Hampel, U. Garreis, F. Jacobi, C. Milczarek, A. Hsieh, K. L. Pulli, B. Chen, J. W. Hoogeboom, S. Bräuer, L. Paulsen, F. P. Schob, S. Schicht, M. |
author_sort | Wittmann, J. |
collection | PubMed |
description | Woundhealing disorders characterized by impaired or delayed re-epithelialization are a serious medical problem that is painful and difficult to treat. Gelsolin (GSN), a known actin modulator, supports epithelial cell regeneration and apoptosis. The aim of this study was to estimate the potential of recombinant gelsolin (rhu-pGSN) for ocular surface regeneration to establish a novel therapy for delayed or complicated wound healing. We analyzed the influence of gelsolin on cell proliferation and wound healing in vitro, in vivo/ex vivo and by gene knockdown. Gelsolin is expressed in all tested tissues of the ocular system as shown by molecular analysis. The concentration of GSN is significantly increased in tear fluid samples of patients with dry eye disease. rhu-pGSN induces cell proliferation and faster wound healing in vitro as well as in vivo/ex vivo. TGF-β dependent transcription of SMA is significantly decreased after GSN gene knockdown. Gelsolin is an inherent protein of the ocular system and is secreted into the tear fluid. Our results show a positive effect on corneal cell proliferation and wound healing. Furthermore, GSN regulates the synthesis of SMA in myofibroblasts, which establishes GSN as a key protein of TGF-β dependent cell differentiation. |
format | Online Article Text |
id | pubmed-6120956 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-61209562018-09-06 Plasma gelsolin promotes re-epithelialization Wittmann, J. Dieckow, J. Schröder, H. Hampel, U. Garreis, F. Jacobi, C. Milczarek, A. Hsieh, K. L. Pulli, B. Chen, J. W. Hoogeboom, S. Bräuer, L. Paulsen, F. P. Schob, S. Schicht, M. Sci Rep Article Woundhealing disorders characterized by impaired or delayed re-epithelialization are a serious medical problem that is painful and difficult to treat. Gelsolin (GSN), a known actin modulator, supports epithelial cell regeneration and apoptosis. The aim of this study was to estimate the potential of recombinant gelsolin (rhu-pGSN) for ocular surface regeneration to establish a novel therapy for delayed or complicated wound healing. We analyzed the influence of gelsolin on cell proliferation and wound healing in vitro, in vivo/ex vivo and by gene knockdown. Gelsolin is expressed in all tested tissues of the ocular system as shown by molecular analysis. The concentration of GSN is significantly increased in tear fluid samples of patients with dry eye disease. rhu-pGSN induces cell proliferation and faster wound healing in vitro as well as in vivo/ex vivo. TGF-β dependent transcription of SMA is significantly decreased after GSN gene knockdown. Gelsolin is an inherent protein of the ocular system and is secreted into the tear fluid. Our results show a positive effect on corneal cell proliferation and wound healing. Furthermore, GSN regulates the synthesis of SMA in myofibroblasts, which establishes GSN as a key protein of TGF-β dependent cell differentiation. Nature Publishing Group UK 2018-09-03 /pmc/articles/PMC6120956/ /pubmed/30177722 http://dx.doi.org/10.1038/s41598-018-31441-2 Text en © The Author(s) 2018 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/. |
spellingShingle | Article Wittmann, J. Dieckow, J. Schröder, H. Hampel, U. Garreis, F. Jacobi, C. Milczarek, A. Hsieh, K. L. Pulli, B. Chen, J. W. Hoogeboom, S. Bräuer, L. Paulsen, F. P. Schob, S. Schicht, M. Plasma gelsolin promotes re-epithelialization |
title | Plasma gelsolin promotes re-epithelialization |
title_full | Plasma gelsolin promotes re-epithelialization |
title_fullStr | Plasma gelsolin promotes re-epithelialization |
title_full_unstemmed | Plasma gelsolin promotes re-epithelialization |
title_short | Plasma gelsolin promotes re-epithelialization |
title_sort | plasma gelsolin promotes re-epithelialization |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6120956/ https://www.ncbi.nlm.nih.gov/pubmed/30177722 http://dx.doi.org/10.1038/s41598-018-31441-2 |
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