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Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions

The pathophysiology of traumatic brain injury (TBI) has not yet been fully elucidated. Crystallin alpha-B (CRYAB) is a molecular chaperone that apparently tries to stabilize the rapid thickening of the intermediate filaments of glial fibrillary acidic protein (GFAP) during the process of reactive as...

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Autores principales: Becerra-Hernández, Lina Vanessa, Escobar-Betancourt, Martha Isabel, Pimienta-Jiménez, Hernán José, Buriticá, Efraín
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8963874/
https://www.ncbi.nlm.nih.gov/pubmed/35360493
http://dx.doi.org/10.3389/fncel.2022.838551
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author Becerra-Hernández, Lina Vanessa
Escobar-Betancourt, Martha Isabel
Pimienta-Jiménez, Hernán José
Buriticá, Efraín
author_facet Becerra-Hernández, Lina Vanessa
Escobar-Betancourt, Martha Isabel
Pimienta-Jiménez, Hernán José
Buriticá, Efraín
author_sort Becerra-Hernández, Lina Vanessa
collection PubMed
description The pathophysiology of traumatic brain injury (TBI) has not yet been fully elucidated. Crystallin alpha-B (CRYAB) is a molecular chaperone that apparently tries to stabilize the rapid thickening of the intermediate filaments of glial fibrillary acidic protein (GFAP) during the process of reactive astrogliosis in response to TBI. Previous analyses of the gene expression profile in human brain contusion tissue showed us an exacerbated CRYAB overexpression. Here, we used 3, 3’-diaminobenzidine (DAB) immunohistochemistry and immunofluorescence to verify CRYAB overexpression and to describe its expression and distribution in samples of contused cortical tissue derived from emergency decompressive surgery after severe TBI. The histological expression of CRYAB was mainly seen in subcortical white matter astrocytes of injured tissue. Most of the cells that overexpressed GFAP in the analyzed tissue also overexpressed CRYAB, a finding corroborated by the co-localization of the two markers. The only difference was the presence of a few pyramidal neurons that expressed CRYAB in layer V of the cerebral cortex. The selective vulnerability of layer V of the cerebral cortex during TBI could explain the expression of CRYAB in neurons of this cortical layer. Our results indicate a parallel behavior in the cellular expression of CRYAB and GFAP during the subacute response to TBI. These results lead us to postulate CRYAB as a possible marker of reactive astrogliosis in contused cortical tissue.
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spelling pubmed-89638742022-03-30 Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions Becerra-Hernández, Lina Vanessa Escobar-Betancourt, Martha Isabel Pimienta-Jiménez, Hernán José Buriticá, Efraín Front Cell Neurosci Cellular Neuroscience The pathophysiology of traumatic brain injury (TBI) has not yet been fully elucidated. Crystallin alpha-B (CRYAB) is a molecular chaperone that apparently tries to stabilize the rapid thickening of the intermediate filaments of glial fibrillary acidic protein (GFAP) during the process of reactive astrogliosis in response to TBI. Previous analyses of the gene expression profile in human brain contusion tissue showed us an exacerbated CRYAB overexpression. Here, we used 3, 3’-diaminobenzidine (DAB) immunohistochemistry and immunofluorescence to verify CRYAB overexpression and to describe its expression and distribution in samples of contused cortical tissue derived from emergency decompressive surgery after severe TBI. The histological expression of CRYAB was mainly seen in subcortical white matter astrocytes of injured tissue. Most of the cells that overexpressed GFAP in the analyzed tissue also overexpressed CRYAB, a finding corroborated by the co-localization of the two markers. The only difference was the presence of a few pyramidal neurons that expressed CRYAB in layer V of the cerebral cortex. The selective vulnerability of layer V of the cerebral cortex during TBI could explain the expression of CRYAB in neurons of this cortical layer. Our results indicate a parallel behavior in the cellular expression of CRYAB and GFAP during the subacute response to TBI. These results lead us to postulate CRYAB as a possible marker of reactive astrogliosis in contused cortical tissue. Frontiers Media S.A. 2022-03-14 /pmc/articles/PMC8963874/ /pubmed/35360493 http://dx.doi.org/10.3389/fncel.2022.838551 Text en Copyright © 2022 Becerra-Hernández, Escobar-Betancourt, Pimienta-Jiménez and Buriticá. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular Neuroscience
Becerra-Hernández, Lina Vanessa
Escobar-Betancourt, Martha Isabel
Pimienta-Jiménez, Hernán José
Buriticá, Efraín
Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title_full Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title_fullStr Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title_full_unstemmed Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title_short Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
title_sort crystallin alpha-b overexpression as a possible marker of reactive astrogliosis in human cerebral contusions
topic Cellular Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8963874/
https://www.ncbi.nlm.nih.gov/pubmed/35360493
http://dx.doi.org/10.3389/fncel.2022.838551
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