Evidence map›Paper›PMID 27393013›Full record

ArticleMetabolic brain disease2016

Delayed bradykinin postconditioning modulates intrinsic neuroprotective enzyme expression in the rat CA1 region after cerebral ischemia: a proteomic study.

Miroslava Nemethova, Ivan Talian, Viera Danielisova, Sona Tkacikova, Petra Bonova, Peter Bober, Milina Matiasova, Jan Sabo, Jozef Burda

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Article in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Miroslava NemethovaInstitute of Neurobiology, SAS, Kosice, Slovakia. nemeth@saske.sk.ORCID 0000-0002-2841-8009
Ivan TalianDepartment of Medical and Clinical Biophysics, Faculty of Medicine, P. J. Safarik University, Kosice, Slovakia.
Viera DanielisovaInstitute of Neurobiology, SAS, Kosice, Slovakia.
Sona TkacikovaDepartment of Medical and Clinical Biophysics, Faculty of Medicine, P. J. Safarik University, Kosice, Slovakia.
Petra BonovaInstitute of Neurobiology, SAS, Kosice, Slovakia.
Peter BoberDepartment of Medical and Clinical Biophysics, Faculty of Medicine, P. J. Safarik University, Kosice, Slovakia.
Milina MatiasovaInstitute of Neurobiology, SAS, Kosice, Slovakia.
Jan SaboDepartment of Medical and Clinical Biophysics, Faculty of Medicine, P. J. Safarik University, Kosice, Slovakia.
Jozef BurdaInstitute of Neurobiology, SAS, Kosice, Slovakia.
University of Pavol Jozef Šafárik · SKInstitute of Neurobiology · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyramidal cells in the CA1 brain region exhibit an ischemic tolerance after delayed postconditioning; therefore, this approach seems to be a promising neuroprotective procedure in cerebral postischemic injury improvement. However, little is known about the effect of postconditioning on protein expression patterns in the brain, especially in the affected hippocampal neurons after global cerebral ischemia. This study is focused on the examination of the ischemia-vulnerable CA1 neuronal layer and on the acquisition of protection from delayed neuronal death after ischemia. Ischemic-reperfusion injury was induced in Wistar rats and bradykinin was applied 2 days after the ischemic insult in an attempt to overcome delayed cell death. Analysis of complex peptide CA1 samples was performed by automated two dimensional liquid chromatography (2D-LC) fractionation coupled to tandem matrix assisted laser desorption/ionization time-of-flight (MALDI TOF/TOF) mass spectrometry instrumentation. We devoted our attention to differences in protein expression mapping in ischemic injured CA1 neurons in comparison with equally affected neurons, but with bradykinin application. Proteomic analysis identified several proteins occurring only after postconditioning and control, which could have a potentially neuroprotective influence on ischemic injured neurons. Among them, the prominent position occupies a regulator of glutamate level aspartate transaminase AATC, a scavenger of glutamate in brain neuroprotection after ischemia-reperfusion. We identified this enzyme in controls and after postconditioning, but AATC presence was not detected in the ischemic injured CA1 region. This finding was confirmed by two-dimensional differential electrophoresis followed by MALDI-TOF/TOF MS identification. Results suggest that bradykinin as delayed postconditioning may be associated with modulation of protein expression after ischemic injury and thus this procedure can be involved in neuroprotective metabolic pathways.

Indexed as

AnimalsBradykininBrain IschemiaCA1 Region, HippocampalGene Expression Regulation, EnzymologicIschemic PostconditioningMaleProteomicsRandom AllocationRatsRats, WistarSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationTime FactorsBradykininCerebral ischemiaHippocampusMALDIPostconditioningProteomicsRat

Identifiers

PMID27393013
OpenAlexW2466796649

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.