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Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues
The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were a...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827060/ https://www.ncbi.nlm.nih.gov/pubmed/33435582 http://dx.doi.org/10.3390/ijms22020591 |
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author | Rath-Deschner, Birgit Nogueira, Andressa Vilas Boas Memmert, Svenja Nokhbehsaim, Marjan Augusto Cirelli, Joni Eick, Sigrun Miosge, Nicolai Kirschneck, Christian Kesting, Marco Deschner, James Jäger, Andreas Damanaki, Anna |
author_facet | Rath-Deschner, Birgit Nogueira, Andressa Vilas Boas Memmert, Svenja Nokhbehsaim, Marjan Augusto Cirelli, Joni Eick, Sigrun Miosge, Nicolai Kirschneck, Christian Kesting, Marco Deschner, James Jäger, Andreas Damanaki, Anna |
author_sort | Rath-Deschner, Birgit |
collection | PubMed |
description | The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost. |
format | Online Article Text |
id | pubmed-7827060 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-78270602021-01-25 Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues Rath-Deschner, Birgit Nogueira, Andressa Vilas Boas Memmert, Svenja Nokhbehsaim, Marjan Augusto Cirelli, Joni Eick, Sigrun Miosge, Nicolai Kirschneck, Christian Kesting, Marco Deschner, James Jäger, Andreas Damanaki, Anna Int J Mol Sci Article The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost. MDPI 2021-01-08 /pmc/articles/PMC7827060/ /pubmed/33435582 http://dx.doi.org/10.3390/ijms22020591 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Rath-Deschner, Birgit Nogueira, Andressa Vilas Boas Memmert, Svenja Nokhbehsaim, Marjan Augusto Cirelli, Joni Eick, Sigrun Miosge, Nicolai Kirschneck, Christian Kesting, Marco Deschner, James Jäger, Andreas Damanaki, Anna Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title | Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title_full | Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title_fullStr | Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title_full_unstemmed | Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title_short | Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues |
title_sort | regulation of anti-apoptotic sod2 and birc3 in periodontal cells and tissues |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827060/ https://www.ncbi.nlm.nih.gov/pubmed/33435582 http://dx.doi.org/10.3390/ijms22020591 |
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