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Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease
The etiology and pathogenesis of rheumatoid arthritis (RA) are marked by a complex interplay of various cell populations and is mediated by different signaling pathways. Traditionally, therapies have primarily focused on pain relief, reducing inflammation and the recovery of joint function. More rec...
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/PMC5733972/ https://www.ncbi.nlm.nih.gov/pubmed/29348703 http://dx.doi.org/10.1155/2017/1046438 |
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author | Tohidnezhad, Mersedeh Bayer, Andreas Rasuo, Biljana Hock, Jennifer Vanessa Phi Kweider, Nisreen Fragoulis, Athanassios Sönmez, Tolga Taha Jahr, Holger Pufe, Thomas Lippross, Sebastian |
author_facet | Tohidnezhad, Mersedeh Bayer, Andreas Rasuo, Biljana Hock, Jennifer Vanessa Phi Kweider, Nisreen Fragoulis, Athanassios Sönmez, Tolga Taha Jahr, Holger Pufe, Thomas Lippross, Sebastian |
author_sort | Tohidnezhad, Mersedeh |
collection | PubMed |
description | The etiology and pathogenesis of rheumatoid arthritis (RA) are marked by a complex interplay of various cell populations and is mediated by different signaling pathways. Traditionally, therapies have primarily focused on pain relief, reducing inflammation and the recovery of joint function. More recently, however, researchers have discussed the therapeutic efficacy of autologous platelet-rich plasma (PRP). The main objective of this work is to examine the influences of platelet-released growth factor (PRGF) on human synoviocytes under inflammatory conditions. Additionally, it is checked to which extend treatment with platelet concentrate influences the release of cytokines form synoviocytes. For this purpose, an in vitro RA model was created by stimulating the cells with the TNF-α. The release of cytokines was measured by ELISA. The cytokine gene expression was analyzed by real-time PCR. It has been observed that the stimulation concentration of 10 ng/ml TNF-α resulted in a significantly increased endogenous secretion and gene expression of IL-6 and TNF-α. The anti-inflammatory effect of PRGF could be confirmed through significant reduction of TNF-α and IL-1β. An induced inflammatory condition seems to cause PRGF to inhibit the release of proinflammatory cytokines. Further study is required to understand the exact effect mechanism of PRGF on synoviocytes. |
format | Online Article Text |
id | pubmed-5733972 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-57339722018-01-18 Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease Tohidnezhad, Mersedeh Bayer, Andreas Rasuo, Biljana Hock, Jennifer Vanessa Phi Kweider, Nisreen Fragoulis, Athanassios Sönmez, Tolga Taha Jahr, Holger Pufe, Thomas Lippross, Sebastian Mediators Inflamm Research Article The etiology and pathogenesis of rheumatoid arthritis (RA) are marked by a complex interplay of various cell populations and is mediated by different signaling pathways. Traditionally, therapies have primarily focused on pain relief, reducing inflammation and the recovery of joint function. More recently, however, researchers have discussed the therapeutic efficacy of autologous platelet-rich plasma (PRP). The main objective of this work is to examine the influences of platelet-released growth factor (PRGF) on human synoviocytes under inflammatory conditions. Additionally, it is checked to which extend treatment with platelet concentrate influences the release of cytokines form synoviocytes. For this purpose, an in vitro RA model was created by stimulating the cells with the TNF-α. The release of cytokines was measured by ELISA. The cytokine gene expression was analyzed by real-time PCR. It has been observed that the stimulation concentration of 10 ng/ml TNF-α resulted in a significantly increased endogenous secretion and gene expression of IL-6 and TNF-α. The anti-inflammatory effect of PRGF could be confirmed through significant reduction of TNF-α and IL-1β. An induced inflammatory condition seems to cause PRGF to inhibit the release of proinflammatory cytokines. Further study is required to understand the exact effect mechanism of PRGF on synoviocytes. Hindawi 2017 2017-11-19 /pmc/articles/PMC5733972/ /pubmed/29348703 http://dx.doi.org/10.1155/2017/1046438 Text en Copyright © 2017 Mersedeh Tohidnezhad et al. http://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 Tohidnezhad, Mersedeh Bayer, Andreas Rasuo, Biljana Hock, Jennifer Vanessa Phi Kweider, Nisreen Fragoulis, Athanassios Sönmez, Tolga Taha Jahr, Holger Pufe, Thomas Lippross, Sebastian Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title | Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title_full | Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title_fullStr | Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title_full_unstemmed | Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title_short | Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease |
title_sort | platelet-released growth factors modulate the secretion of cytokines in synoviocytes under inflammatory joint disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733972/ https://www.ncbi.nlm.nih.gov/pubmed/29348703 http://dx.doi.org/10.1155/2017/1046438 |
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