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Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes
Autologous thrombocyte concentrate lysates, for example, platelet-released growth factors, (PRGFs) or their clinically related formulations (e.g., Vivostat PRF®) came recently into the physicians' focus as they revealed promising effects in regenerative and reparative medicine such as the suppo...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541813/ https://www.ncbi.nlm.nih.gov/pubmed/28808357 http://dx.doi.org/10.1155/2017/5671615 |
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author | Bayer, Andreas Tohidnezhad, Mersedeh Lammel, Justus Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Jahr, Holger Cremer, Jochen Rademacher, Franziska Gläser, Regine Harder, Jürgen |
author_facet | Bayer, Andreas Tohidnezhad, Mersedeh Lammel, Justus Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Jahr, Holger Cremer, Jochen Rademacher, Franziska Gläser, Regine Harder, Jürgen |
author_sort | Bayer, Andreas |
collection | PubMed |
description | Autologous thrombocyte concentrate lysates, for example, platelet-released growth factors, (PRGFs) or their clinically related formulations (e.g., Vivostat PRF®) came recently into the physicians' focus as they revealed promising effects in regenerative and reparative medicine such as the support of healing of chronic wounds. To elucidate the underlying mechanisms, we analyzed the influence of PRGF and Vivostat PRF on human keratinocyte differentiation in vitro and on epidermal differentiation status of skin wounds in vivo. Therefore, we investigated the expression of early (keratin 1 and keratin 10) and late (transglutaminase-1 and involucrin) differentiation markers. PRGF treatment of primary human keratinocytes decreased keratin 1 and keratin 10 gene expression but induced involucrin and transglutaminase-1 gene expression in an epidermal growth factor receptor- (EGFR-) dependent manner. In concordance with these results, microscopic analyses revealed that PRGF-treated human keratinocytes displayed morphological features typical of keratinocytes undergoing terminal differentiation. In vivo treatment of artificial human wounds with Vivostat PRF revealed a significant induction of involucrin and transglutaminase-1 gene expression. Together, our results indicate that PRGF and Vivostat PRF induce terminal differentiation of primary human keratinocytes. This potential mechanism may contribute to the observed beneficial effects in the treatment of hard-to-heal wounds with autologous thrombocyte concentrate lysates in vivo. |
format | Online Article Text |
id | pubmed-5541813 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-55418132017-08-14 Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes Bayer, Andreas Tohidnezhad, Mersedeh Lammel, Justus Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Jahr, Holger Cremer, Jochen Rademacher, Franziska Gläser, Regine Harder, Jürgen Mediators Inflamm Research Article Autologous thrombocyte concentrate lysates, for example, platelet-released growth factors, (PRGFs) or their clinically related formulations (e.g., Vivostat PRF®) came recently into the physicians' focus as they revealed promising effects in regenerative and reparative medicine such as the support of healing of chronic wounds. To elucidate the underlying mechanisms, we analyzed the influence of PRGF and Vivostat PRF on human keratinocyte differentiation in vitro and on epidermal differentiation status of skin wounds in vivo. Therefore, we investigated the expression of early (keratin 1 and keratin 10) and late (transglutaminase-1 and involucrin) differentiation markers. PRGF treatment of primary human keratinocytes decreased keratin 1 and keratin 10 gene expression but induced involucrin and transglutaminase-1 gene expression in an epidermal growth factor receptor- (EGFR-) dependent manner. In concordance with these results, microscopic analyses revealed that PRGF-treated human keratinocytes displayed morphological features typical of keratinocytes undergoing terminal differentiation. In vivo treatment of artificial human wounds with Vivostat PRF revealed a significant induction of involucrin and transglutaminase-1 gene expression. Together, our results indicate that PRGF and Vivostat PRF induce terminal differentiation of primary human keratinocytes. This potential mechanism may contribute to the observed beneficial effects in the treatment of hard-to-heal wounds with autologous thrombocyte concentrate lysates in vivo. Hindawi 2017 2017-07-20 /pmc/articles/PMC5541813/ /pubmed/28808357 http://dx.doi.org/10.1155/2017/5671615 Text en Copyright © 2017 Andreas Bayer et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Bayer, Andreas Tohidnezhad, Mersedeh Lammel, Justus Lippross, Sebastian Behrendt, Peter Klüter, Tim Pufe, Thomas Jahr, Holger Cremer, Jochen Rademacher, Franziska Gläser, Regine Harder, Jürgen Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title | Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title_full | Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title_fullStr | Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title_full_unstemmed | Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title_short | Platelet-Released Growth Factors Induce Differentiation of Primary Keratinocytes |
title_sort | platelet-released growth factors induce differentiation of primary keratinocytes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541813/ https://www.ncbi.nlm.nih.gov/pubmed/28808357 http://dx.doi.org/10.1155/2017/5671615 |
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