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Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells
BACKGROUND: Dental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines beco...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448245/ https://www.ncbi.nlm.nih.gov/pubmed/31041893 http://dx.doi.org/10.1186/s12860-019-0185-4 |
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author | Morsczeck, Christian Reck, Anja Reichert, Torsten E. |
author_facet | Morsczeck, Christian Reck, Anja Reichert, Torsten E. |
author_sort | Morsczeck, Christian |
collection | PubMed |
description | BACKGROUND: Dental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines become senescent at different rates. We hypothesized that short telomere length and increased DNA damage with genomic instability correlate with the accelerated induction of cellular senescence. RESULTS: For this study we compared DFC cell lines that became senescent at different rates (DFC_F: strong senescent phenotype; DFC_S: weak senescent phenotype). The telomeres of DFC_F were shorter than those of the telomeres of DFC_S prior senescence. Interestingly, telomere lengths of both cell lines were nearly unchanged after induction of senescence. Gene expression analyses with genes associated with DNA damage before and after the induction of cellular senescence revealed that almost all genes in DFCs_F were down-regulated while the gene expression in DFC_S was almost constitutive. Moreover, number of aneuploid DFC_F were significantly higher after induction of cellular senescence. CONCLUSION: Our results supported our initial hypothesis that telomere length and genomic instability correlate with the accelerated induction of cellular senescence in DFC_F. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12860-019-0185-4) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6448245 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-64482452019-05-01 Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells Morsczeck, Christian Reck, Anja Reichert, Torsten E. BMC Mol Cell Biol Research Article BACKGROUND: Dental follicle cells (DFCs) are dental stem cells and interesting options for regenerative therapies in dentistry. However, DFCs acquire replicative senescence in long-term cultures, but little is known about molecular processes. In previous studies, we observed that DFC cell lines become senescent at different rates. We hypothesized that short telomere length and increased DNA damage with genomic instability correlate with the accelerated induction of cellular senescence. RESULTS: For this study we compared DFC cell lines that became senescent at different rates (DFC_F: strong senescent phenotype; DFC_S: weak senescent phenotype). The telomeres of DFC_F were shorter than those of the telomeres of DFC_S prior senescence. Interestingly, telomere lengths of both cell lines were nearly unchanged after induction of senescence. Gene expression analyses with genes associated with DNA damage before and after the induction of cellular senescence revealed that almost all genes in DFCs_F were down-regulated while the gene expression in DFC_S was almost constitutive. Moreover, number of aneuploid DFC_F were significantly higher after induction of cellular senescence. CONCLUSION: Our results supported our initial hypothesis that telomere length and genomic instability correlate with the accelerated induction of cellular senescence in DFC_F. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12860-019-0185-4) contains supplementary material, which is available to authorized users. BioMed Central 2019-04-03 /pmc/articles/PMC6448245/ /pubmed/31041893 http://dx.doi.org/10.1186/s12860-019-0185-4 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Morsczeck, Christian Reck, Anja Reichert, Torsten E. Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title | Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title_full | Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title_fullStr | Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title_full_unstemmed | Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title_short | Short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
title_sort | short telomeres correlate with a strong induction of cellular senescence in human dental follicle cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448245/ https://www.ncbi.nlm.nih.gov/pubmed/31041893 http://dx.doi.org/10.1186/s12860-019-0185-4 |
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