Abstract
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.
Highlights
Traumatic brain injury (TBI) is a phenomenon that involves a direct injury caused at the time of the event, as well as injuries caused by secondary damage in the aftermath of the event, which are closely related to trauma sequels and patient outcome
The similarity in counts of Glial Fibrillary Acidic Protein (GFAP)- and Crystallin alpha-B (CRYAB)-positive cells, as well as the cellular colocalization of both markers found in this study, allow us to propose CRYAB as a possible alternative histological biomarker of reactive astrogliosis in TBI
Reactive astroglia are characterized by increased cell size and the production of cytoskeletal intermediate filaments; for this reason, GFAP labeling has been widely used to identify this process in a variety of central nervous system disorders, including TBI (Sofroniew, 2009; Sofroniew and Vinters, 2010; Burda and Sofroniew, 2014; Pekny and Pekna, 2014; Liddelow and Barres, 2017)
Summary
Traumatic brain injury (TBI) is a phenomenon that involves a direct injury caused at the time of the event (primary damage), as well as injuries caused by secondary damage in the aftermath of the event, which are closely related to trauma sequels and patient outcome. Various cellular and molecular events involved in the establishment and progress of secondary damage due to trauma have been described (Maas, 2016; O’Leary and Nichol, 2018). The phenomenon of reactive astrogliosis is one of these events, during which changes in glial cells in response to injury can be seen. Astrocytes are a type of glial cell. They are abundant in the nervous system, with functions related to the maintenance of tissue homeostasis, and the isolation of synaptic clefts.
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