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Hypertension exacer...
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Czigler, AndrasDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary
(författare)
Hypertension exacerbates cerebrovascular oxidative stress induced by mild traumatic brain injury : Protective effects of the Mitochondria-Targeted Antioxidative Peptide SS-31
- Artikel/kapitelEngelska2019
Förlag, utgivningsår, omfång ...
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Mary Ann Liebert,2019
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Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:oru-113619
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-113619URI
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https://doi.org/10.1089/neu.2019.6439DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
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Funding Agencies:National Research, Development & Innovation Office (NRDIO)Hungarian Academy of Sciences Bolyai Research Scholarship3/2016 04.01/FNew National Excellence Program of the Ministry of Human Capacities, Higher Education Institutional Excellence ProgrammeHungarian National Brain Research ProgramMarie Curie ActionsUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute on Aging R01-AG047879United States Department of Health & Human ServicesNIH National Institute of Neurological Disorders & Stroke (NINDS)
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Traumatic brain injury (TBI) induces cerebrovascular oxidative stress, which is associated with neurovascular uncoupling, autoregulatory dysfunction, and persisting cognitive decline in both pre-clinical models and patients. However, single mild TBI (mTBI), the most frequent form of brain trauma, increases cerebral generation of reactive oxygen species (ROS) only transiently. We hypothesized that comorbid conditions might exacerbate long-term ROS generation in cerebral arteries after mTBI. Because hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive and spontaneously hypertensive rats (SHR) and assessed changes in cytoplasmic and mitochondrial superoxide (O2-) production by confocal microscopy in isolated middle cerebral arteries (MCA) 2 weeks after mTBI using dihydroethidine (DHE) and the mitochondria-targeted redox-sensitive fluorescent indicator dye MitoSox. We found that mTBI induced a significant increase in long-term cytoplasmic and mitochondrial O2- production in MCAs of SHRs and increased expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit Nox4, which were reversed to the normal level by treating the animals with the cell-permeable, mitochondria-targeted antioxidant peptide SS-31 (5.7 mg kg-1 day-1, i.p.). Persistent mTBI-induced oxidative stress in MCAs of SHRs was significantly decreased by inhibiting vascular NADPH oxidase (apocyinin). We propose that hypertension- and mTBI-induced cerebrovascular oxidative stress likely lead to persistent dysregulation of cerebral blood flow (CBF) and cognitive dysfunction, which might be reversed by SS-31 treatment.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Toth, LucaDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary
(författare)
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Szarka, NikolettInstitute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary
(författare)
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Berta, GergelyMedical Biology and University of Pecs, Medical School, Pecs, Hungary
(författare)
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Amrein, KriszitinaDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary
(författare)
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Czeiter, EndreDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Immunology and Biotechnology, University of Pecs, Medical School, Pecs, Hungary
(författare)
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Lendvai-Emmert, DominikaDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary
(författare)
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Bodo, KorneliaImmunology and Biotechnology, University of Pecs, Medical School, Pecs, Hungary
(författare)
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Tarantini, StefanoReynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
(författare)
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Koller, AkosDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Department of Morphology and Physiology, Semmelweis University, Budapest, Hungary; Sport-Physiology Research Center, University of Physical Education, Budapest, Hungary; Department of Physiology, New York Medical College, Valhalla, New York, USA
(författare)
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Ungvari, ZoltanReynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
(författare)
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Büki, Andras,1966-Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary(Swepub:oru)asbi
(författare)
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Toth, PeterDepartment of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary
(författare)
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Department of Neurosurgery and Szentagothai Research Center, University of Pecs, Medical School, Pecs, Hungary; Institute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, HungaryInstitute for Translational Medicine, Departments of University of Pecs, Medical School, Pecs, Hungary
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Journal of Neurotrauma: Mary Ann Liebert36:23, s. 3309-33150897-71511557-9042
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Czigler, Andras
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Toth, Luca
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Szarka, Nikolett
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Berta, Gergely
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Amrein, Krisziti ...
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Czeiter, Endre
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Lendvai-Emmert, ...
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Bodo, Kornelia
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Tarantini, Stefa ...
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Koller, Akos
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Ungvari, Zoltan
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Büki, Andras, 19 ...
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Toth, Peter
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- MEDICIN OCH HÄLSOVETENSKAP
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och Klinisk medicin
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