TY - JOUR
T1 - Crystallin Alpha-B Overexpression as a Possible Marker of Reactive Astrogliosis in Human Cerebral Contusions
AU - Becerra-Hernández, Lina Vanessa
AU - Escobar-Betancourt, Martha Isabel
AU - Pimienta-Jiménez, Hernán José
AU - Buriticá, Efraín
N1 - Publisher Copyright:
Copyright © 2022 Becerra-Hernández, Escobar-Betancourt, Pimienta-Jiménez and Buriticá.
PY - 2022/3/14
Y1 - 2022/3/14
N2 - 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.
AB - 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.
KW - CRYAB
KW - brain contusion
KW - crystallin alpha B
KW - glial fibrillary acidic protein (GFAP)
KW - human cerebral cortex
KW - reactive gliosis (astrogliosis)
KW - severe traumatic brain injury (TBI)
KW - αB-crystallin
UR - http://www.scopus.com/inward/record.url?scp=85127560569&partnerID=8YFLogxK
U2 - 10.3389/fncel.2022.838551
DO - 10.3389/fncel.2022.838551
M3 - Article
AN - SCOPUS:85127560569
SN - 1662-5102
VL - 16
JO - Frontiers in Cellular Neuroscience
JF - Frontiers in Cellular Neuroscience
M1 - 838551
ER -