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Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation
Intracellular Flightless I (Flii), a gelsolin family member, has been found to have roles modulating actin regulation, transcriptional regulation and inflammation. In vivo Flii can regulate wound healing responses. We have recently shown that a pool of Flii is secreted by fibroblasts and macrophages...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541319/ https://www.ncbi.nlm.nih.gov/pubmed/23336022 http://dx.doi.org/10.4161/cib.21928 |
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author | Cowin, Allison J. Lei, Nazi Franken, Linda Ruzehaji, Nadira Offenhäuser, Carolin Kopecki, Zlatko Murray, Rachael Z. |
author_facet | Cowin, Allison J. Lei, Nazi Franken, Linda Ruzehaji, Nadira Offenhäuser, Carolin Kopecki, Zlatko Murray, Rachael Z. |
author_sort | Cowin, Allison J. |
collection | PubMed |
description | Intracellular Flightless I (Flii), a gelsolin family member, has been found to have roles modulating actin regulation, transcriptional regulation and inflammation. In vivo Flii can regulate wound healing responses. We have recently shown that a pool of Flii is secreted by fibroblasts and macrophages, cells typically found in wounds, and its secretion can be upregulated upon wounding. We show that secreted Flii can bind to the bacterial cell wall component lipopolysaccharide and has the potential to regulate inflammation. We now show that secreted Flii is present in both acute and chronic wound fluid. |
format | Online Article Text |
id | pubmed-3541319 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-35413192013-01-18 Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation Cowin, Allison J. Lei, Nazi Franken, Linda Ruzehaji, Nadira Offenhäuser, Carolin Kopecki, Zlatko Murray, Rachael Z. Commun Integr Biol Short Communication Intracellular Flightless I (Flii), a gelsolin family member, has been found to have roles modulating actin regulation, transcriptional regulation and inflammation. In vivo Flii can regulate wound healing responses. We have recently shown that a pool of Flii is secreted by fibroblasts and macrophages, cells typically found in wounds, and its secretion can be upregulated upon wounding. We show that secreted Flii can bind to the bacterial cell wall component lipopolysaccharide and has the potential to regulate inflammation. We now show that secreted Flii is present in both acute and chronic wound fluid. Landes Bioscience 2012-11-01 /pmc/articles/PMC3541319/ /pubmed/23336022 http://dx.doi.org/10.4161/cib.21928 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Short Communication Cowin, Allison J. Lei, Nazi Franken, Linda Ruzehaji, Nadira Offenhäuser, Carolin Kopecki, Zlatko Murray, Rachael Z. Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title | Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title_full | Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title_fullStr | Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title_full_unstemmed | Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title_short | Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation |
title_sort | lysosomal secretion of flightless i upon injury has the potential to alter inflammation |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541319/ https://www.ncbi.nlm.nih.gov/pubmed/23336022 http://dx.doi.org/10.4161/cib.21928 |
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