A Single Primary Blast-Induced Traumatic Brain Injury in a Rodent Model Causes Cell-Type Dependent Increase in Nicotinamide Adenine Dinucleotide Phosphate Oxidase Isoforms in Vulnerable Brain Regions.
A Single Primary Blast-Induced Traumatic Brain Injury in a Rodent Model Causes Cell-Type Dependent Increase in Nicotinamide Adenine Dinucleotide Phosphate Oxidase Isoforms in Vulnerable Brain Regions.
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DOI：
10.1089/neu.2017.5358
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发表时间：
2018-09-01
影响因子：
4.2
通讯作者：
Chandra N
中科院分区：
文献类型：
--
作者：
Rama Rao KV;Iring S;Younger D;Kuriakose M;Skotak M;Alay E;Gupta RK;Chandra N
爆炸引起的创伤性脑损伤（bTBI）是战场上和训练场所中具有长期神经和心理病理学的士兵发病的主要原因。我们实验室以前的研究表明，爆炸伤后氧化应激途径的激活，但它们在不同脑区之间的分布及其对bTBI发病机制的影响尚未探讨。本研究探讨了两种亚型的蛋白质表达：烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶1和2（NOX 1，NOX 2），相应的超氧化物的产生，NOX激活的下游事件，和4-羟基壬烯醛（4 HNE）的脂质过氧化加合物的范围内的蛋白质。在冲击波暴露后4 h评价脑损伤，并在不同脑区域进行免疫荧光信号定量。NOX亚型的表达在不同的脑区显示出差异性的增加：在海马和丘脑中，NOX 1的增加最多，而在额叶皮层中，NOX 2的表达增加最多。细胞特异性分析相对于相应的控制NOX表达的变化显示，爆炸导致在神经元中的NOX 1和NOX 2水平的增加更高的星形胶质细胞和小胶质细胞相比。爆炸暴露也导致不同脑区超氧化物水平增加，这种变化反映在4 HNE蛋白加合物的形成。总的来说，这项研究表明，原发性冲击波TBI诱导脑实质不同区域的NADPH氧化酶亚型上调，并且与其他神经细胞相比，神经元似乎面临更高的氧化损伤风险。
Blast-induced traumatic brain injury (bTBI) is a leading cause of morbidity in soldiers on the battlefield and in training sites with long-term neurological and psychological pathologies. Previous studies from our laboratory demonstrated activation of oxidative stress pathways after blast injury, but their distribution among different brain regions and their impact on the pathogenesis of bTBI have not been explored. The present study examined the protein expression of two isoforms: nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 and 2 (NOX1, NOX2), corresponding superoxide production, a downstream event of NOX activation, and the extent of lipid peroxidation adducts of 4-hydroxynonenal (4HNE) to a range of proteins. Brain injury was evaluated 4 h after the shock-wave exposure, and immunofluorescence signal quantification was performed in different brain regions. Expression of NOX isoforms displayed a differential increase in various brain regions: in hippocampus and thalamus, there was the highest increase of NOX1, whereas in the frontal cortex, there was the highest increase of NOX2 expression. Cell-specific analysis of changes in NOX expression with respect to corresponding controls revealed that blast resulted in a higher increase of NOX1 and NOX 2 levels in neurons compared with astrocytes and microglia. Blast exposure also resulted in increased superoxide levels in different brain regions, and such changes were reflected in 4HNE protein adduct formation. Collectively, this study demonstrates that primary blast TBI induces upregulation of NADPH oxidase isoforms in different regions of the brain parenchyma and that neurons appear to be at higher risk for oxidative damage compared with other neural cells.
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影响因子：
9.3
作者：
Dohi K;Ohtaki H;Nakamachi T;Yofu S;Satoh K;Miyamoto K;Song D;Tsunawaki S;Shioda S;Aruga T
通讯作者：
Aruga T
延迟的MGLUR5激活限制了创伤性脑损伤后神经炎症和神经退行性的限制。
影响因子：
9.3
作者：
Byrnes KR;Loane DJ;Stoica BA;Zhang J;Faden AI
通讯作者：
Faden AI
影响因子：
--
作者：
Bandak, F A;Ling, G;De Lanerolle, N C
通讯作者：
De Lanerolle, N C
DOI：
10.1016/j.cbpc.2010.06.001
发表时间：
2010-09-01
影响因子：
3.9
作者：
Banakou, Eleni;Dailianis, Stefanos
通讯作者：
Dailianis, Stefanos
影响因子：
4.8
作者：
FERNANDEZ, V;BARRIENTOS, X;VIDELA, LA
通讯作者：
VIDELA, LA