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Traumatic brain injury impairs myogenic constriction of cerebral arteries : role of mitochondria-derived H2O2 and TRPV4-dependent activation of BKca Channels

Szarka, Nikolett (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Neurotrauma Research Group, Janos Szentagothai Research Center, Medical School University of Pecs, Pecs, Hungary; Department of Translational Medicine, Medical School University of Pecs, Pecs, Hungary
Pabbidi, Mallikarjuna R. (author)
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, USA
Amrein, Krisztina (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Neurotrauma Research Group, Janos Szentagothai Research Center, Medical School University of Pecs, Pecs, Hungary
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Czeiter, Endre (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Neurotrauma Research Group, Janos Szentagothai Research Center, Medical School University of Pecs, Pecs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary
Berta, Gergely (author)
Department of Medical Biology, Medical School University of Pecs, Pecs, Hungary
Pohoczky, Krisztina (author)
Department of Pharmacology and Pharmacotherapy, Medical School University of Pecs, Pecs, Hungary; MTA-PTE NAP B Chronic Pain Research Group, Pecs, Hungary
Helyes, Zsuzsanna (author)
Department of Pharmacology and Pharmacotherapy, Medical School University of Pecs, Pecs, Hungary; MTA-PTE NAP B Chronic Pain Research Group, Pecs, Hungary
Ungvari, Zoltan (author)
Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Koller, Akos (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Institute of Natural Sciences, University of Physical Education, Budapest, Hungary; Department of Physiology, New York Medical College, Valhalla, New York, USA
Büki, Andras, 1966- (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Neurotrauma Research Group, Janos Szentagothai Research Center, Medical School University of Pecs, Pecs, Hungary
Toth, Peter (author)
Cerebrovascular Laboratory, Department of Neurosurgery, Medical School University of Pecs, Pecs, Hungary; Neurotrauma Research Group, Janos Szentagothai Research Center, Medical School University of Pecs, Pecs, Hungary; Department of Translational Medicine, Medical School University of Pecs, Pecs, Hungary; MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary; Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
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 (creator_code:org_t)
Mary Ann Liebert, 2018
2018
English.
In: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 35:7, s. 930-939
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Traumatic brain injury (TBI) impairs autoregulation of cerebral blood flow, which contributes to the development of secondary brain injury, increasing mortality of patients. Impairment of pressure-induced myogenic constriction of cerebral arteries plays a critical role in autoregulatory dysfunction; however, the underlying cellular and molecular mechanisms are not well understood. To determine the role of mitochondria-derived H2O2 and large-conductance calcium-activated potassium channels (BKCa) in myogenic autoregulatory dysfunction, middle cerebral arteries (MCAs) were isolated from rats with severe weight drop-impact acceleration brain injury. We found that 24 h post-TBI MCAs exhibited impaired myogenic constriction, which was restored by treatment with a mitochondria-targeted antioxidant (mitoTEMPO), by scavenging of H2O2 (polyethylene glycol [PEG]-catalase) and by blocking both BKCa channels (paxilline) and transient receptor potential cation channel subfamily V member 4 (TRPV4) channels (HC 067047). Further, exogenous administration of H2O2 elicited significant dilation of MCAs, which was inhibited by blocking either BKCa or TRPV4 channels. Vasodilation induced by the TRPV4 agonist GSK1016790A was inhibited by paxilline. In cultured vascular smooth muscle cells H2O2 activated BKCa currents, which were inhibited by blockade of TRPV4 channels. Collectively, our results suggest that after TBI, excessive mitochondria-derived H2O2 activates BKCa channels via a TRPV4-dependent pathway in the vascular smooth muscle cells, which impairs pressure-induced constriction of cerebral arteries. Future studies should elucidate the therapeutic potential of pharmacological targeting of this pathway in TBI, to restore autoregulatory function in order to prevent secondary brain damage and decrease mortality.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

Keyword

Autoregulation
intracranial hypertension
oxidative stress
secondary injury

Publication and Content Type

ref (subject category)
art (subject category)

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