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Cell-Free Mitochondrial DNA in Acute Brain Injury

Traumatic brain injury and aneurysmal subarachnoid haemorrhage are a major cause of morbidity and mortality worldwide. Treatment options remain limited and are hampered by our understanding of the cellular and molecular mechanisms, including the inflammatory response observed in the brain. Mitochond...

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Autores principales: Kayhanian, Saeed, Glynos, Angelos, Mair, Richard, Lakatos, Andras, Hutchinson, Peter J.A., Helmy, Adel E., Chinnery, Patrick F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mary Ann Liebert, Inc., publishers 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9531878/
https://www.ncbi.nlm.nih.gov/pubmed/36204389
http://dx.doi.org/10.1089/neur.2022.0032
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author Kayhanian, Saeed
Glynos, Angelos
Mair, Richard
Lakatos, Andras
Hutchinson, Peter J.A.
Helmy, Adel E.
Chinnery, Patrick F.
author_facet Kayhanian, Saeed
Glynos, Angelos
Mair, Richard
Lakatos, Andras
Hutchinson, Peter J.A.
Helmy, Adel E.
Chinnery, Patrick F.
author_sort Kayhanian, Saeed
collection PubMed
description Traumatic brain injury and aneurysmal subarachnoid haemorrhage are a major cause of morbidity and mortality worldwide. Treatment options remain limited and are hampered by our understanding of the cellular and molecular mechanisms, including the inflammatory response observed in the brain. Mitochondrial DNA (mtDNA) has been shown to activate an innate inflammatory response by acting as a damage-associated molecular pattern (DAMP). Here, we show raised circulating cell-free (ccf) mtDNA levels in both cerebrospinal fluid (CSF) and serum within 48 h of brain injury. CSF ccf-mtDNA levels correlated with clinical severity and the interleukin-6 cytokine response. These findings support the use of ccf-mtDNA as a biomarker after acute brain injury linked to the inflammatory disease mechanism.
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spelling pubmed-95318782022-10-05 Cell-Free Mitochondrial DNA in Acute Brain Injury Kayhanian, Saeed Glynos, Angelos Mair, Richard Lakatos, Andras Hutchinson, Peter J.A. Helmy, Adel E. Chinnery, Patrick F. Neurotrauma Rep Original Article Traumatic brain injury and aneurysmal subarachnoid haemorrhage are a major cause of morbidity and mortality worldwide. Treatment options remain limited and are hampered by our understanding of the cellular and molecular mechanisms, including the inflammatory response observed in the brain. Mitochondrial DNA (mtDNA) has been shown to activate an innate inflammatory response by acting as a damage-associated molecular pattern (DAMP). Here, we show raised circulating cell-free (ccf) mtDNA levels in both cerebrospinal fluid (CSF) and serum within 48 h of brain injury. CSF ccf-mtDNA levels correlated with clinical severity and the interleukin-6 cytokine response. These findings support the use of ccf-mtDNA as a biomarker after acute brain injury linked to the inflammatory disease mechanism. Mary Ann Liebert, Inc., publishers 2022-09-28 /pmc/articles/PMC9531878/ /pubmed/36204389 http://dx.doi.org/10.1089/neur.2022.0032 Text en © Saeed Kayhanian et al., 2022; Published by Mary Ann Liebert, Inc. https://creativecommons.org/licenses/by/4.0/This Open Access article is distributed under the terms of the Creative Commons License [CC-BY] (http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kayhanian, Saeed
Glynos, Angelos
Mair, Richard
Lakatos, Andras
Hutchinson, Peter J.A.
Helmy, Adel E.
Chinnery, Patrick F.
Cell-Free Mitochondrial DNA in Acute Brain Injury
title Cell-Free Mitochondrial DNA in Acute Brain Injury
title_full Cell-Free Mitochondrial DNA in Acute Brain Injury
title_fullStr Cell-Free Mitochondrial DNA in Acute Brain Injury
title_full_unstemmed Cell-Free Mitochondrial DNA in Acute Brain Injury
title_short Cell-Free Mitochondrial DNA in Acute Brain Injury
title_sort cell-free mitochondrial dna in acute brain injury
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9531878/
https://www.ncbi.nlm.nih.gov/pubmed/36204389
http://dx.doi.org/10.1089/neur.2022.0032
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