Traumatic brain injury and autophagy: a pilot study about the immunohistochemical expression of LC3B, Beclin 1, p62, and LAMP2A in human autoptic samples.

IF 3.5 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2025-04-28 eCollection Date: 2025-01-01 DOI:10.3389/fnmol.2025.1562954
Tommaso Livieri, Letizia Alfieri, Emiliana Giacomello, Djordje Alempijević, Tijana Petrovic, Yanko Georgiev Kolev, Davide Radaelli, Margherita Neri, Stefano D'Errico
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引用次数: 0

Abstract

Introduction: Autophagy is a cellular stress response that has been shown in the literature to be active in cerebral cells after a traumatic brain injury (TBI). The aim of this study is to investigate the potential use of four proteins involved in autophagy (LC3B, Beclin 1, p62, and LAMP2A), as a forensic diagnostic marker for TBI.

Methods: We analyzed histological samples obtained from the frontal lobe of 10 subjects who died within 1 h of a TBI (Group A), 13 who died between 1 h and 32 days post-TBI (Group B), and a control group of 10 subjects who died without head trauma (Group C). Immunohistochemical (IHC) staining using anti-LC3B, anti-Beclin 1, anti-p62 and anti-LAMP2A antibodies was performed.

Results and discussion: The results show that LC3B staining was the only one that show a statistically significant difference between groups. In particular, the percentage of neurons displaying an autophagic pattern was calculated from six random acquisitions per subject, and the results were compared across groups using one way ANOVA. Significant differences were observed between Groups A and B, and between Groups B and C, with p-values of 0.0055 and 0.0035, respectively. While the difference between Groups A and C was not statistically significant (p-value of 0.9845). These findings suggest that LC3B may serve as a useful diagnostic marker for TBI in cases where death is not immediate and open the door for further research.

外伤性脑损伤与自噬:LC3B、Beclin 1、p62、LAMP2A在人自噬样本中免疫组化表达的初步研究
导读:自噬是一种细胞应激反应,文献显示创伤性脑损伤(TBI)后脑细胞活跃。本研究的目的是研究参与自噬的四种蛋白(LC3B, Beclin 1, p62和LAMP2A)作为TBI法医诊断标志物的潜在用途。方法:我们分析了10例TBI后1小时内死亡的受试者(a组),13例TBI后1 h至32 天死亡的受试者(B组)和10例无头部创伤死亡的对照组(C组)的额叶组织学样本。采用抗lc3b、抗beclin 1、抗p62和抗lamp2a抗体进行免疫组化(IHC)染色。结果与讨论:结果显示LC3B染色是组间唯一有统计学差异的染色。特别是,显示自噬模式的神经元的百分比是从每个受试者的六个随机获取中计算出来的,并使用单向方差分析比较各组的结果。A组与B组、B组与C组间差异显著,p值分别为0.0055和0.0035。而A组与C组间差异无统计学意义(p值为0.9845)。这些发现表明,LC3B可能作为TBI病例中一个有用的诊断标志物,并为进一步的研究打开了大门。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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