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The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence

Pharmacological interventions for traumatic brain injury (TBI) are limited. Together with parvalbumin (PV) loss, increased production of reactive oxygen species (ROS) by the NADPH oxidase NOX enzymes represents a key step in TBI. Here, we investigated the contribution of NOX2-derived oxidative stres...

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Autores principales: Schiavone, Stefania, Neri, Margherita, Trabace, Luigia, Turillazzi, Emanuela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562735/
https://www.ncbi.nlm.nih.gov/pubmed/28821783
http://dx.doi.org/10.1038/s41598-017-09202-4
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author Schiavone, Stefania
Neri, Margherita
Trabace, Luigia
Turillazzi, Emanuela
author_facet Schiavone, Stefania
Neri, Margherita
Trabace, Luigia
Turillazzi, Emanuela
author_sort Schiavone, Stefania
collection PubMed
description Pharmacological interventions for traumatic brain injury (TBI) are limited. Together with parvalbumin (PV) loss, increased production of reactive oxygen species (ROS) by the NADPH oxidase NOX enzymes represents a key step in TBI. Here, we investigated the contribution of NOX2-derived oxidative stress to the loss of PV immunoreactivity associated to TBI, performing immunohistochemistry for NOX2, 8-hydroxy-2′-deoxyguanosine (8OHdG) and PV on post mortem brain samples of subjects died following TBI, subjects died from spontaneous intracerebral hemorrhage (SICH) and controls (CTRL). We detected an increased NOX2 expression and 8OHdG immunoreactivity in subjects died from TBI with respect to CTRL and SICH. NOX2 increase was mainly observed in GABAergic PV-positive interneurons, with a minor presence in microglia. No significant differences in other NADPH oxidase isoforms (NOX1 and NOX4) were detected among experimental groups. NOX2-derived oxidative stress elevation appeared a specific TBI-induced phenomenon, as no alterations in the nitrosative pathway were detected. Our results suggest that NOX2-derived oxidative stress might play a crucial role in the TBI-induced loss of PV-positive interneurons.
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spelling pubmed-55627352017-08-21 The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence Schiavone, Stefania Neri, Margherita Trabace, Luigia Turillazzi, Emanuela Sci Rep Article Pharmacological interventions for traumatic brain injury (TBI) are limited. Together with parvalbumin (PV) loss, increased production of reactive oxygen species (ROS) by the NADPH oxidase NOX enzymes represents a key step in TBI. Here, we investigated the contribution of NOX2-derived oxidative stress to the loss of PV immunoreactivity associated to TBI, performing immunohistochemistry for NOX2, 8-hydroxy-2′-deoxyguanosine (8OHdG) and PV on post mortem brain samples of subjects died following TBI, subjects died from spontaneous intracerebral hemorrhage (SICH) and controls (CTRL). We detected an increased NOX2 expression and 8OHdG immunoreactivity in subjects died from TBI with respect to CTRL and SICH. NOX2 increase was mainly observed in GABAergic PV-positive interneurons, with a minor presence in microglia. No significant differences in other NADPH oxidase isoforms (NOX1 and NOX4) were detected among experimental groups. NOX2-derived oxidative stress elevation appeared a specific TBI-induced phenomenon, as no alterations in the nitrosative pathway were detected. Our results suggest that NOX2-derived oxidative stress might play a crucial role in the TBI-induced loss of PV-positive interneurons. Nature Publishing Group UK 2017-08-18 /pmc/articles/PMC5562735/ /pubmed/28821783 http://dx.doi.org/10.1038/s41598-017-09202-4 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Schiavone, Stefania
Neri, Margherita
Trabace, Luigia
Turillazzi, Emanuela
The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title_full The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title_fullStr The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title_full_unstemmed The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title_short The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
title_sort nadph oxidase nox2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562735/
https://www.ncbi.nlm.nih.gov/pubmed/28821783
http://dx.doi.org/10.1038/s41598-017-09202-4
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