Cargando…

Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury

Previous results on nitric oxide (NO) metabolism after traumatic brain injury (TBI) show variations in NO availability and controversial effects of exogenous nitric oxide synthase (NOS)-inhibitors. Furthermore, elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) were r...

Descripción completa

Detalles Bibliográficos
Autores principales: Jung, Carla S., Wispel, Christian, Zweckberger, Klaus, Beynon, Christopher, Hertle, Daniel, Sakowitz, Oliver W., Unterberg, Andreas W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975386/
https://www.ncbi.nlm.nih.gov/pubmed/24663083
http://dx.doi.org/10.3390/ijms15034088
_version_ 1782310141966680064
author Jung, Carla S.
Wispel, Christian
Zweckberger, Klaus
Beynon, Christopher
Hertle, Daniel
Sakowitz, Oliver W.
Unterberg, Andreas W.
author_facet Jung, Carla S.
Wispel, Christian
Zweckberger, Klaus
Beynon, Christopher
Hertle, Daniel
Sakowitz, Oliver W.
Unterberg, Andreas W.
author_sort Jung, Carla S.
collection PubMed
description Previous results on nitric oxide (NO) metabolism after traumatic brain injury (TBI) show variations in NO availability and controversial effects of exogenous nitric oxide synthase (NOS)-inhibitors. Furthermore, elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) were reported in cerebro-spinal fluid (CSF) after traumatic subarachnoid hemorrhage (SAH). Therefore, we examined whether ADMA and the enzymes involved in NO- and ADMA-metabolism are expressed in brain tissue after TBI and if time-dependent changes occur. TBI was induced by controlled cortical impact injury (CCII) and neurological performance was monitored. Expression of NOS, ADMA, dimethylarginine dimethylaminohydrolases (DDAH) and protein-arginine methyltransferase 1 (PRMT1) was determined by immunostaining in different brain regions and at various time-points after CCII. ADMA and PRMT1 expression decreased in all animals after TBI compared to the control group, while DDAH1 and DDAH2 expression increased in comparison to controls. Furthermore, perilesionally ADMA is positively correlated with neuroscore performance, while DDAH1 and DDAH2 are negatively correlated. ADMA and its metabolizing enzymes show significant temporal changes after TBI and may be new targets in TBI treatment.
format Online
Article
Text
id pubmed-3975386
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher Molecular Diversity Preservation International (MDPI)
record_format MEDLINE/PubMed
spelling pubmed-39753862014-04-04 Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury Jung, Carla S. Wispel, Christian Zweckberger, Klaus Beynon, Christopher Hertle, Daniel Sakowitz, Oliver W. Unterberg, Andreas W. Int J Mol Sci Article Previous results on nitric oxide (NO) metabolism after traumatic brain injury (TBI) show variations in NO availability and controversial effects of exogenous nitric oxide synthase (NOS)-inhibitors. Furthermore, elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) were reported in cerebro-spinal fluid (CSF) after traumatic subarachnoid hemorrhage (SAH). Therefore, we examined whether ADMA and the enzymes involved in NO- and ADMA-metabolism are expressed in brain tissue after TBI and if time-dependent changes occur. TBI was induced by controlled cortical impact injury (CCII) and neurological performance was monitored. Expression of NOS, ADMA, dimethylarginine dimethylaminohydrolases (DDAH) and protein-arginine methyltransferase 1 (PRMT1) was determined by immunostaining in different brain regions and at various time-points after CCII. ADMA and PRMT1 expression decreased in all animals after TBI compared to the control group, while DDAH1 and DDAH2 expression increased in comparison to controls. Furthermore, perilesionally ADMA is positively correlated with neuroscore performance, while DDAH1 and DDAH2 are negatively correlated. ADMA and its metabolizing enzymes show significant temporal changes after TBI and may be new targets in TBI treatment. Molecular Diversity Preservation International (MDPI) 2014-03-06 /pmc/articles/PMC3975386/ /pubmed/24663083 http://dx.doi.org/10.3390/ijms15034088 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Jung, Carla S.
Wispel, Christian
Zweckberger, Klaus
Beynon, Christopher
Hertle, Daniel
Sakowitz, Oliver W.
Unterberg, Andreas W.
Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title_full Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title_fullStr Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title_full_unstemmed Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title_short Endogenous Nitric-Oxide Synthase Inhibitor ADMA after Acute Brain Injury
title_sort endogenous nitric-oxide synthase inhibitor adma after acute brain injury
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975386/
https://www.ncbi.nlm.nih.gov/pubmed/24663083
http://dx.doi.org/10.3390/ijms15034088
work_keys_str_mv AT jungcarlas endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT wispelchristian endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT zweckbergerklaus endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT beynonchristopher endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT hertledaniel endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT sakowitzoliverw endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury
AT unterbergandreasw endogenousnitricoxidesynthaseinhibitoradmaafteracutebraininjury