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Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum
Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following pers...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6411151/ https://www.ncbi.nlm.nih.gov/pubmed/30856215 http://dx.doi.org/10.1371/journal.pone.0213673 |
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author | Tominaga, Tadasuke Shimada, Ryo Okada, Yoshikazu Kawamata, Takakazu Kibayashi, Kazuhiko |
author_facet | Tominaga, Tadasuke Shimada, Ryo Okada, Yoshikazu Kawamata, Takakazu Kibayashi, Kazuhiko |
author_sort | Tominaga, Tadasuke |
collection | PubMed |
description | Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage response signaling, leading to cell disorders. TBI initially activates the cell cycle followed by the subsequent triggering of senescence. This study aims to clarify how the mRNA and protein expression of different markers of cell cycle and senescence are modulated and switched over time after TBI. We performed senescence-associated-β-galactosidase (SA-β-gal) staining, immunohistochemical analysis, and real-time PCR to examine the time-dependent changes in expression levels of proteins and mRNA, related to cell cycle and cellular senescence markers, in the cerebrum during the initial 14 days after TBI using a mouse model of controlled cortical impact (CCI). Within the area adjacent to the cerebral contusion after TBI, the protein and/or mRNA expression levels of cell cycle markers were increased significantly until 4 days after injury and senescence markers were significantly increased at 4, 7, and 14 days after injury. Our findings suggested that TBI initially activated the cell cycle in neurons, astrocytes, and microglia within the area adjacent to the hemicerebrum contusion in TBI, whereas after 4 days, such cells could undergo senescence in a cell-type-dependent manner. |
format | Online Article Text |
id | pubmed-6411151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-64111512019-04-01 Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum Tominaga, Tadasuke Shimada, Ryo Okada, Yoshikazu Kawamata, Takakazu Kibayashi, Kazuhiko PLoS One Research Article Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage response signaling, leading to cell disorders. TBI initially activates the cell cycle followed by the subsequent triggering of senescence. This study aims to clarify how the mRNA and protein expression of different markers of cell cycle and senescence are modulated and switched over time after TBI. We performed senescence-associated-β-galactosidase (SA-β-gal) staining, immunohistochemical analysis, and real-time PCR to examine the time-dependent changes in expression levels of proteins and mRNA, related to cell cycle and cellular senescence markers, in the cerebrum during the initial 14 days after TBI using a mouse model of controlled cortical impact (CCI). Within the area adjacent to the cerebral contusion after TBI, the protein and/or mRNA expression levels of cell cycle markers were increased significantly until 4 days after injury and senescence markers were significantly increased at 4, 7, and 14 days after injury. Our findings suggested that TBI initially activated the cell cycle in neurons, astrocytes, and microglia within the area adjacent to the hemicerebrum contusion in TBI, whereas after 4 days, such cells could undergo senescence in a cell-type-dependent manner. Public Library of Science 2019-03-11 /pmc/articles/PMC6411151/ /pubmed/30856215 http://dx.doi.org/10.1371/journal.pone.0213673 Text en © 2019 Tominaga et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Tominaga, Tadasuke Shimada, Ryo Okada, Yoshikazu Kawamata, Takakazu Kibayashi, Kazuhiko Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title | Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title_full | Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title_fullStr | Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title_full_unstemmed | Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title_short | Senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
title_sort | senescence-associated-β-galactosidase staining following traumatic brain injury in the mouse cerebrum |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6411151/ https://www.ncbi.nlm.nih.gov/pubmed/30856215 http://dx.doi.org/10.1371/journal.pone.0213673 |
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