Literature DB >> 22301378

Quantitative analysis of GFAP- and S100 protein-immunopositive astrocytes to investigate the severity of traumatic brain injury.

Dong-Ri Li1, Fu Zhang, Yao Wang, Xiao-Hui Tan, Dong-Fang Qiao, Hui-Jun Wang, Tomomi Michiue, Hitoshi Maeda.   

Abstract

Previous studies have shown that diffuse cortical astrocyte damage is seen in acute deaths due to brain injury and mechanical asphyxiation. The present study quantitatively investigated the number of astrocytes that showed GFAP- and S100-protein immunopositivity in the cerebral white matter and hippocampus at the sites distant from primary injury with regard to survival time, complication, and the immediate cause of death of brain injury cases. Autopsy cases of brain injury (8-48 h postmortem) comprising acute/subacute deaths (survival time, <3/6 h-3 days; n=27/42) and delayed deaths (survival time >3 days) with/without complications (n=30/22) were examined. Delayed death cases with complications were subdivided into those in which the immediate cause of death had been determined as cerebral dysfunction (n=22) and those that had been determined as due to fatal complications (n=8). For controls, natural deaths from pneumonias (n=12) and sudden cardiac deaths (n=27) were used. In brain injury cases, the numbers of astrocytes in the cerebral white matter and hippocampal CA4 region were significantly lower for subacute death and delayed death without complications (p<0.05-0.001). Delayed death with fatal complications showed a significant increase in the number of astrocytes (p<0.05). Among delayed death cases, the numbers of astrocytes were higher in the cases with fatal complications than in those without complications and with non-fatal complications, although the latter cases showed large variations in the numbers of these astrocytes. These findings suggest that critical brain injury causes acute death without evident astrocyte pathology and that subacute death is associated with progressive brain damage accompanied by an astrocyte loss. In delayed death cases, the numbers astrocytes might be closely related to the severity of posttraumatic brain injury. GFAP and S100-immunopositivity might be useful for elucidating the cause and process of deaths due to brain injury.
Copyright © 2012. Published by Elsevier Ireland Ltd.

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Year:  2012        PMID: 22301378     DOI: 10.1016/j.legalmed.2011.12.007

Source DB:  PubMed          Journal:  Leg Med (Tokyo)        ISSN: 1344-6223            Impact factor:   1.376


  11 in total

1.  Traumatically injured astrocytes release a proteomic signature modulated by STAT3-dependent cell survival.

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Journal:  Int J Legal Med       Date:  2015-04-07       Impact factor: 2.686

3.  New astroglial injury-defined biomarkers for neurotrauma assessment.

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Journal:  Neurochem Res       Date:  2018-10-24       Impact factor: 3.996

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6.  Addressing the needs of traumatic brain injury with clinical proteomics.

Authors:  Sean Shen; Rachel R Ogorzalek Loo; Ina-Beate Wanner; Joseph A Loo
Journal:  Clin Proteomics       Date:  2014-03-28       Impact factor: 3.988

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Journal:  Sci Rep       Date:  2018-02-05       Impact factor: 4.379

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Journal:  J Neuroinflammation       Date:  2020-12-14       Impact factor: 8.322

9.  Effects of antioxidant treatment on blast-induced brain injury.

Authors:  Xiaoping Du; Donald L Ewert; Weihua Cheng; Matthew B West; Jianzhong Lu; Wei Li; Robert A Floyd; Richard D Kopke
Journal:  PLoS One       Date:  2013-11-05       Impact factor: 3.240

10.  Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization.

Authors:  Catalina Lapuente Chala; Carlos Augusto Rengifo Valbuena; Marco Fidel Avila Rodríguez; Angel Céspedes Rubio
Journal:  Colomb Med (Cali)       Date:  2013-03-30
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